IV induction/Neuro monitoring/Inhalation hx/volatiles Flashcards
what are examples of adjunct medications to primary anesthetics
antihistamines
antipsychotics
benzodiazipines
opioids
what is balanced anesthesia
premedication
light sedation
regional anesthesia
what is general anesthesia
balance of unconsciousness, analgesia, amnesia, suppression of stress response, immobility
-unarousable complete loss of consciousness
-inability to maintain airway control
-loss of eyelid reflex
what pathway do the majority of IV inductions agents on on
excitement of inhibitory signals through the gamma-aminobutyric acid type A (GABA) receptors
what are MOA theories
-membrane protein binding sites
-alter signaling between neurons (charges)
-GABA: ligand gated ion channels
what receptors does ketamine work on
NMDA
receptors contain multiple
subunits
what is the primary binding site on GABA, what is the effect
GABA 2, hyper polarization
GABA is an ______ neurotransmitter
inhibitory
what are examples of excitatory neurotransmitters
acetylcholine
glutamate
what are examples of secondary IV induction agents
Antihistamines
antipsychotics
benzodiazepines
opioids
what is general anesthesia
A balance of unconsciousness, analgesia, amnesia, suppression of the stress
response, and sufficient immobility
T/F general anesthesia results in an unarousable state and complete loss of consciousness
True
T/F general anesthesia results in an inability to maintain airway or controll reflexes
true
T/F general anesthesia results in the loss of eyelid reflexes
true
what are the MOA theories for IV induction agents
-membrane protein binding sites
-altering signaling between neurons by altering ion channels
-GABA receptors
where do the majority of IV induction agents act (receptor)
enhancement of inhibitory signals through the gamma-aminobutyric
acid type A (GABA) receptors
what system do most IV induction agents have their action on
reticular activating system in brainstem
what does the reticular activating system control
consciousness
what controls the signals coming into the reticular activating system? where does it send the message
thalamus
cerebral cortex
what neurotransmitter does the reticular activating system use
acetycholine
what kind of feedback mechanism does the reticular activating system use
positive feedback
what are examples of excitatory neurotransmitters
acetylcholine
dopamine
norepinephrine
glutamate
what are examples of inhibitory neurotransmitters
Gamma-aminobutyric acid (GABA)
what is the most abundant inhibitory neurotransmitter in the brain
GABA
what does GABAa regulate
neuronal excitability
what does GABAa mediate
unconsciousness, amnesia, suppression of spinal reflexes
what channels does GABA work on
Ligand-gated ion cys-loop channels
how many protein subunits make up a GABA receptor
5
what channel does the GABA receptor control? what is the affect of its activation?
Cl-
hyperpolarization
what controls the release of GABA
Ca++
what happens when GABA is activated
-increases Cl- conductance
-cell membrane hyperpolarization
-decreased neuronal excitability
where on GABA receptor does the GABAa endogenous enzyme bind
alpha and beta subunit
where on GABAa receptor do Benzodiazepines bind
alpha and gamma subunits
where on GABAa receptor does propofol, etomidate, and barbituates bind
within or proximal to beta subunits
suppression of NMDA receptors leads to
depression of neuronal activity
Where are NMDA receptors found
pre, post, and extra synaptically
how many subunits are in an NMDA receptor
4 around a central ion channel pore
what types of subunits are NMDA receptors made from
-an NR1 receptor
-4 types of NR2 subunits (A-d)
-NR3
what effects the onset of an NMDA receptor
presynaptic glutamate
voltage of membrane
what blocks the channel pore of an NMDA receptor if agonist is present
Mg++
NMDA receptors play a significant role in CNS functions that require activity-dependent changes in cellular physiology such as
learning and processing of sensory information
what is an example of an NMDA antagonist
ketamine
IV induction agents that work on NMDA are
antagonists
IV induction agents that work on GABA receptors are
agonists
does ketamine competitively or non-competitively bind to NMDA receptrs
non-competitive
Ketamine can only bind to NMDA receptors that are in the _________ position
open
what are examples of barbituate IV induction agents
thiopental,
Methohexital (brevital),
Pentobarbitol
T/F brevital changes the seizure threshold
False
what receptors do barbituates work on
GABA
block action of Glutamate at AMPA and Kainate
inhibits neuronal nicotinic receptors
how do barbiturates affects GABAa receptor
Enhances GABAa receptor function and decreases the rate of disassociation of GABA
T/F barbituates block glutamate at NMDA receptors
false
how do high doses of barbiturates affect GABA receptors
directly activate GABA receptors (even in absence of GABA)
T/F barbiturates cause EEG changes
T, cause low to high frequency patterns on EEG
the CNS depression caused by barbiturates is ________ dependent
dose
barbiturates ________ cerebral metabolic rate for O2 (CMRO2) by _____ %
decrease
55%
which barbiturates have anticonvulsant properties
Thiopental
pentobarbital
barbiturates cause veno____________
dilation
barbiturates (increase/decrease) preload and CO
decrease
what conditions do you avoid barbiturates in and why
aortic stenosis/tamponade
decreased preload and CO
do you mix barbiturates with ROC
no
do you mix barbiturates with saline?
why?
no
will precipitate
what order of kinetics do barbiturates go thorugh
first order unless there is a high concentration
barbiturates are weak (acids/bases)
acids
barbiturates require a pH>_____ to remain aquas
10
what happens if you mix barbiturates in non-base solutions like N.S and L.R.
precipitate
barbiturates become ________philic in plasma
lipophilic
what is the onset of barbiturates? why?
30-60 seconds
readily pronate in plasma and become lipophilic
60% of barbiturates are __________ (ionized/non-ionized) at body pH due to pKa being higher.
this results in (easy/difficult) passage through lipid membranes
non-ionized
easy
what terminates the initial dose of barbiturates
redistribution
Vd of barbiturates is related to perfusion of what
vessel rich organs
muscles results in a _______ reservoir
large
fat results in a ______ reservoir
smaller, slow distribution
Barbiturates are (high/low) protein bound
highly 75-90
if a patient has liver disease how does this effect your barbiturate dose
decrease it
how are barbiturates metabolized
liver
T/F barbiturates cause histamine release
true
what are s/s histamine release
uticarial rash
anaphylaxis
Hives
Edema
Bronchospasm
Shock
which barbiturate causes pain on injection
methohexital
what happens with IV infiltration of barbiturates
severe tissue necrosis
what can happen with intra-arterial injection of barbiturates
chemical endarteritis
destroys tissue
intense vasospasm
excruciating pain
necrosis/gangrene
permanent nerve damage
what are signs of the intense vasospasm caused by intra-arterial injection of barbiturates
blanching of skin with disappearance of pulses
what is the induction dose of methohexital
1 mg/kg
what is the sedation dose of methohexital
0.2-0.4 mg/kg
what is the duration of induction dose of methohexital
5-10 min
what is the 1/2 life methohexital
3.9 hrs
what is the pediatric rectal dose of methohexital
25 mg/kg
what conditions is etomidate useful for
cardiac (aortic stenosis, tamponade, sepsis)
what IV induction agent has the greatest selectivity for GABAa
Etomidate
how many enantiomer are in etomidate? why?
1
R(+) isomer having the greatest hypnotic effects
T/F Etomidate is hydrophilic
F, it is lipophilic
T/F Etomidate is highly protein bound
true
how long does it take Etomidate to reach peak brain levels
2 min
how is Etomidate metabolized
liver
Plasma esterases
how is the end product of etomidate metabolism excreted
renal
what can Etomidate inhibit
11b-hydroxylase in the adrenal cortex, causes adrenal corticol suppression
what is the induction dose of Etomidate
0.2-0.4 mg/kg
what is the T1/2 of Etomidate
2.9 hrs
what is the onset/peak/DOA of Etomidate
30s/1 min/3-10 min
what is the Vd of Etomidate
2-4.5 L/kg
what is the CL of Etomidate
10-20 mL/kg/min
how does etomidate affect EEG
EEG slows to burst suppression
how does etomidate affect CMRO2
decreases
how does etomidate affecrt resp
resp depression
which causes more resp depression prop or etomidate
propofol
how does etomidate affect muscles, how do you mitigate this
myoclonus, inject slowly
how does etomidate affect injection site
pain on injection
thrombophlebitis
how does etomidate affect venous system
minimal vasodilation
in what conditions can etomidate still cause significant vasodilation
sepsis,
shock,
SVR <2500,
aortic stenosis
how does etomidate affect cardiac
minimal cardiac depression
how does etomidate affect GI
n/v
T/F etomidate is an anticonvulsant
true
what is 2,6 diisopropylphenol
propofol
What is MOA of propofol
-Potentiates GABA-mediated responses
-directly activates GABAA receptor
What GABA subunits does etomidate bind to?
likely b
T/F propofol is a weak base
false
its a weak acid
T/F propofol is lipophilic
true
T/F propofol is a chiral molecule
F, it is achiral
propofol is formulated in a lipid emulsion to mitigate its
hydrophobia
what is the lipid emulsion of propofol formulated from
soybean oil,
glycerol,
purified egg phospholipid (lecithin)
T/F egg allergy crossover is common in propfol
f its rare
how long can an open vial or syringe of prop be open before disposal
12 hrs
how long can propofol be in a syringe before it is thrown away
1-2 hrs
what is in prop to stop bacterial growth
an antimicrobial
what are examples of antimicrobials in propofol
ethylenediaminetetraacetic acid or sodium metabisulfite
what causes the pain in propofol injection
its free aqueous concentration
how can you mitigate pain of propofol injection
use AC vein
coadmin with lidocaine
what causes propofols rapid onset
lipid solubility
young people require (more/less) propofol
more
how is propofol metabolized
liver
how is propofol excreted
renal
what is CL of propofol
25 ml/kg/min
T/F moderate hepatic or renal impairment has a large effect on DOA of propofol
F, it is little effect
what causes the short DOA of propofol
rapid redistribution
what is the induction dose of propofol
2-2.5 mg/kg
what is the induction dose of propofol for >65 yo
1-1.5 mg/kg
what is the onset/peak/doa of propofol
60 s, 1 min, 5-10 min
what is the elimination 1/2 life of propofol
0.5-1.5 hrs
what is the Vd of propofol
2-10 L/kg
do you use propofol in sepsis
no
how much do you lower propofol dose by in sever hypovolemia
80-90%
if you fluid resuscitate a hypovolemic patient patient how much do you decrease prop dose by
50%
how does propofol affect EEG
slows to burst suppression
how does propofol affect CMRO2
decreases
how does propofol affect airway muscles
decreases reflexes and tone
how does propofol affect heart
myocardial depression
how does propofol affect muscles
rhabdomyolysis with infusion syndrome (rare)
how does propofol affect liver
hypertriglyceridemia with prolonged infusions
how does propofol affect injection site
pain on injection
how does propofol affect venous system
decreased vascular resistance
how does propofol affect lungs
bronchodilation, resp depression
how does propofol affect GI
antiemesis
T/F propofol is an anticonvulsant
true
what is the only IV induction drug that decreases pain
ketamine
what kind of drug is Ketamine
NMDA receptor antagonist
what kind of mixture is ketamine
racemic mixture of R and S enantiomers
T/F ketamine is competitive binding
false
what other receptor does ketamine block
nicotinic
what gives ketamine its local anesthetic properties
Na+ channels and binds mu and k opioid receptors
what are common clinical uses of ketamine
OB/C section
T/F Ketamine depresses RAS
false
T/F ketamine dissociates thalamus from limbic cortex
true
how does ketamine affect CMRO2, CBF, and ICP
increases
T/F ketamine is a good drug for head trauma patients
F, it increases ICP
what are emergence reactions from ketamine
unpleasant hallucination,
vivid dreams,
delirium
how can you reduce the incidence of emergence reactions with ketamine
benzos
how does ketamine affect IOP
increases, dont give in glaucoma
do you use ketamine in open eye injuries
no, increases IOP
T/F nystagmus is common in ketamine
true
what is the induction dose of Ketamine
1-2mg/kg IV or
4-8 mg/kg IM
what is the onset/peak/doa of ketamine
30s/1min/5-15 min
what is the elimination 1/2 life of ketamine
2-3 hours
what is the Vd of Ketamine
2.5-3.5 L/kg
what is the CL of ketamine
17 ml/kg/min
how does ketamine affect venous system
increased vascular resistance
What are the CNS effects of ketamine?
dissociative sedation
possible emergence delirium
how doe ketamine affect eyes
nystagmus
how does ketamine affect mouth
increased salivation
what drugs can you used to decrease salivation
glyco
IV scoplamine
how does ketamine affect lungs
bronchodilation with preserved resp drive
how does ketamine affect heart
indirect myocardial stimulation
direct myocardial depression
what are the “good” effects of ketamine
maintains SVR
increased HR
bronchodilation
awake intubations
maintain resp drive
local mac on sick patient
what are the “Bad” effects of ketamine
dont use on head traumas
dont use on eye traumas
dont use in cardiac or aortic stenosis 2/2 tachycardia
what does too much muscle relaxant lead to
longer recovery phase
prolonged mechanical ventilation
increased expense to institution
what is the last muscle to be paralyzed and the first to wake up
diaphragm
can a muscle fiber partially contract?
no it is all or none
the response of the entire muscle depends on
the # of nerves activated
what is a supramaximal stimulus
> 50 mA, +20-25% of necessary, so painful
when do we use supramaximal stimulus
when patient is asleep
when do we use submaximal stimulus
when patient is awake
what is the number of cycles/)second of electrical stimulation (how rapidly a stimulation occurs)
Hz (hertz)
what is 0.1 Hz
one stimuli every 10 seconds
what is 1.0 Hz
one stimuli every second
the electricity during PNA stimulation is _______
constant
what are the 2 variables of Peripheral nerve stimulator
Hz-how often stimuli is applied
mA- electrical output, how much electricity
what percent of patients experience residual paralysis
50%
what patients do not notice residual paralysis
young healthy
what patients suffer from residual paralysis
obese, emphysema
what do you give patients suffering from residual paralysis
reversal like sugammadex or neostig
where do we place the red electrode for monitoring
directly over nerve, toward head
where do we place the black electrode for monitoring
directly over nerve, distal
what does an electrical current cause to be released
an action potential releases ACh at the synaptic cleft
what are the different patterns of nerve stimulation
single twitch
TOF (train of four)
Tetanus
Post-tetanic count (PTC)
Double-burst stimulation (DBS)
how do you use TOF
compare T1 to T4 and make ratio/percentage
how do we use tetanus
constant shock, watch for fade
in a phase 2 block if you do 5 seconds of tetany and there is no fade what does this tell you
you are safe to extubate
what is benefit of DBS
more accurate supposedly
when single twitch stimulation results in no twitches what muscles have been relaxed
laryngeal and diaphragm
what do you have to do before using the single twitch stimulation method
require baseline stimulation prior to NMBA given
how long does a single twitch stimulation last
0.2 msec
how often does TOF give stimuli
every 0.5 seconds (2 Hz)
what is the frequency of TOF
2Hz
how is TOF evaluated
fade
how is TOF ratio determined
twitches/4
T4/T1
how do you determine TOF %
T4/T1
if there is NO neuromuscular blockade the 4th twitch will feel the same as the ______
1st
as neuromuscular blockade increases, 4th twitch__________ until it ________
decreases
disappears
after 4th twitch is lost what twitch is lost next
3rd then 2nd
what is the optimal # of twitches
1-2
with deep neuromuscular blockade how many twitches are present
none
when is TOF most sensitive
70-100% paralysis
the 4th twitch in TOF disappears at _________ blockade
75-80%
the 3rd twitch in TOF disappears at _________ blockade
80-85%
the 2nd twitch in TOF disappears at _________ blockade
90-95%
what is considered the ideal operative paralysis %
85-95% blockade, 1-2 twitches
how many twitches are present at 75-80% blockade
3
how many twitches are present at 80-85% blockade
2
how many twitches are present at 90-95% blockade
1
what percent block is this
<70%
what percent block is this
75%
what percent block is this
80
what percent block is this
90%
what percent block is this
100%
what are advantages of TOF
less painful
degree of block in nondepolarizing block can be evaluated
good for assessing surgical relaxation
what is a phase one block
depolarization
what is a depolarizing drug
Succinylcholine
what happens with a high dose of succs
phase 2 block
how does train of four appear in depolarizing blocks
all twitches are the same so all strong, all weak, or all gone
which block has muscle fasciculation
depolarizing/phase 1
which block has sustained response to tetanic stimulation
depolarizing/phase 1
which block has absence of posttetanic potentiation, stimulation, or facilitation
depolarizing/phase 1
which block has a lack of fade to tetanus, train of four, and double burst stimulation
depolarizing/phase 1
which block is antagonized by prior admin of nondeplarizer as pretreatment
depolarizing/phse 1
which block is potentiated by anticholinesterase drugs
depolarizing/phase 1
which block has an absence of muscle fasciculation
nondepolarizing/phase 2
which block has the appearance of tetanic fade and posttetanic potentiation, stimulation, or facilitation
nondepolarizing/phase 2
which block has TOF and double burst fade
nondepolarizing/phase 2
which block is reversible with anticholinesterase drugs
nondepolarizing/phase 2
which block can be produced by an overdose and desensitization with succs at doses greater than 6 mg/kg
nondeplarizing/phase 2
what does a TOF with succs look like
what order do twitches reappear in
same order the disappear
what is the TOF response of non-depolarizing block
what is TOF response of depolarizing block
what TOF indicates adequate recovery
0.7
what does a TOF ratio of 0.7 mean
4th twitch is 70% as strong as 1st twitch
at a TOF of 0.7 patients should be able to maintain ___________
airway
at TOF of 0.7 ther are enough unoccupied receptors to bind with
Ach
at what Hz does can tetanic stimulation deliver shock
30, 50, or 100
what is the most common shock for tetanic stimulation
50 Hz for 5 seconds or 100 Hz for 5 seconds
what are we observing for in tetanic stimulation
fade
what is the physiology behind fade
presynaptic event
at beginning of tetanus large Ach released from nerve terminal
as stores are depleted the rate of release of Ach is depleted
what does the degree of fade depend on
degree of neuromuscular blockade
frequency (Hz)
length (seconds)
how often tetanic stimulation is applied
what causes fade in tetany
receptors are still occupied by NDMR
what is the best shock indicator for extubation
5 second tetany, fade is easy to see
50 Hz is _________ shocks per second OR one shock every ___________
50
20 msec
100 Hz is _________ shocks per second OR one shock every ___________
100
10 msec
does fade occur in depolarizing muscle relaxant
no
if a patient is completely blocked with succs how will tetanus appear
no contraction
if patient is partially blocked with succs how will tetanus appear
weak contraction that does not get weaker
what do you do if you blocked a patient with an NDMR and you get no response to TOF
count post tetanic twitches
-shock 50 Hz for 5 sec then wait 3 seconds then do a single twitch stimuli at 1 Hz
post tetanic twitches will appear __________ the first twitch in TOF. This is called ________
before
post tetanic potentiation
what is the Hz and interval of Double burst stimulation
two bursts of 50 Hz separated by 750 msec
how does double burst stimulation appear in nonparalyzed muscle
2 equal contractions
how does double stimulation appear in partially paralyzed muscle
2nd response is weaker than first
how many receptors are occupied when a patient has a tidal volume of 5 ml/kg
80% (20% free)
how many receptors are occupied when a patient has no palpable fade to TOF stimulation
70-75% (25-30% free)
how many receptors are occupied with sustained tetanus at 50 Hz for 5 sec
70% (30% free)
how many receptors are occupied with vital capacity of 20 ml/kg
70% (30% free)
how many receptors are occupied when there is no palpable fade with double-burst stimulation
60-70% (30-40% free)
how many receptors are occupied when inspiratory force reaches -40 cm H2O
50% (50% free)
how many receptors are occupied when patient can lift head for 5 sec
50%
how many receptors are occupied with sustained hand grip
50%
how many receptors are occupied with sustained bite and jaw clench on tongue blade
50%
what peripheral nerves are used for stimulation
ulnar nerve
orbicularis oculi
corrugator supercilii
orbicularis oris
posterior tibial nerve
common peroneal nerve
median nerve
T/F ulnar nerve is well correlated with larynx and diaphragm
false
what response are you looking for when shocking ulnar nerve
thumb adduction
what response are you looking for when shocking facial nerves
eyelid and eyebrow movement
what is benefit of ulnar nerve site
easy access
what is benefit of facial nerve site
easily accessed when arm not available
best site to measure onset (paralyzed first)
which is more resistant to relaxants corrugator supercilli or orbicularis oculi
corrugator supercilii (eyebrow muscle)
the diaphragm requires ________ times the amount required to black the adductor pollicis muscle
1.4-2x
which recovers faster the diaphragm or adductor pllicis
diaphragm
a surgeon is complaining that the patient is pushing, so you check twitches on the adductor pollicis and the patient is blocked, what is happening
diaphragm takes more drug to paralyze and comes off faster
list muscles from the most to least sensitive to blockade
abd
orbicularis oculi
geniohyoid
masseter
upper airway muscles
peripheral limbs
laryngeal
diphragm
where should red electrode be placed on arm
ulnar groove
the inner eyebrow is _________ sensitive than the outer eyebrow
less
facial stimulation sites
when does intense blockade happen after giving an intubating dose of a NDMR
3-6min
do you reverse during total blockade?
no
what is another name for surgical blockade
moderate blockade
how many twitches are present during an intense blockade
none
when does moderate/surgical blockade begin
when 1st twitch of TOF returns
how many twitches are present during surgical blockade
1-2
T/F patients cannot cough or buck during surgical blockade
false
can you reverse during surgical/moderate blockade
yes
how many receptors are blocked with complete paralysis, 0/4 TOF
99-100
how many receptors are blocked when diaphragm moves 0/4 TOF
95
how many receptors are blocked with abdominal relaxation is adequate 1/4 TOF
90
how many receptors are blocked when TV and VC are normal and 4/4 TOF
75% (25% free)
how many receptors are blocked when patient can inspire -20 cm H2O and head lift is sustained
50%
how many receptors are blocked when hand grasp is sustained
30% (70% free)
sevoflurane belongs to which anesthetic drug class
ethers (C-O-C)
vapor pressure
the pressure exerted by a vapor in equilibrium with its liquid or solid phase inside of a closed container
directly proportional to temp
increased temp= increased vapor pressure
vapor pressure is _____(less than/greater than) atmospheric pressure
less than
what occurs when vapor pressure is equal to atmospheric pressure?
boiling
what can transform volatile anesthetics into toxic compounds?
CO2 absorbent and the liver
what is not stable in hydrated soda lime
sevo
produces compound A
what does des and iso make if they become unstable in desiccated soda lime
carbon monoxide (des>iso)
vapor pressure of sevo
160
vapor pressure of des
660
vapor pressure of iso
238
vapor pressure of N2O
38,770
boiling point of sevo
59*C
boiling point of des
22*c
boiling point of iso
49*C
boiling point of N2O
-88*c
what is the molecular weight of sevo
200g
molecular weight of des
168g
molecular weight of iso
184g
molecular weight of N2O
44g
what anesthetics are stable in hydrated CO2 absorber
des
iso
N2O
what anesthetics are stable in dehydrated CO2 absorber
N2O
what is the blood:gas partial coefficient of des
0.42
what is the blood:gas partial coefficient of N2O
0.47
what is the blood:gas partial coefficient of sevo
0.6
what is the blood:gas partial coefficient of iso
1.4
define the blood: gas coefficient
the ability of the anesthetic agent to dissolve into the blood and tissues;
the relative solubility of an inhalation anesthetic in the blood vs alveolar gas when partial pressures between the two compartments are equal
a polar solute will be more soluble in a ____
hydrophilic solvent
a non polar solute will be more soluble in a ______
lipophilic solvent
an anesthetic gas with low blood:gas solubility is _____ likely to be taken up in the blood
LESS
oil : gas sevo
50
oil : gas des
18.7
oil : gas iso
99
oil : gas N2O
1.4
what three factors determine anesthetic uptake into the blood
agent solubility
partial pressure difference between alveoli and the blood
cardiac output
low solubility = _____ equilibration of FA/FI
faster
this means faster onset
high solubility = _____equilibration of FA/FI
slower
means slower onset
FA is determined by what two factors
delivery from anesthesia machine to alveoli
rate of transfer from alveoli to the blood
what affects the delivery from anesthesia machine to alveoli
setting on the vaporizer
time constant of delivery system
anatomic dead space
alveolar ventilation
volume of the FRC
what affects the rate of transfer from alveoli to the blood
blood: gas solubility
cardiac output
what factors increase FA/FI
increase wash in:
-high FGF
-high alveolar ventilation
-low FRC
-low time constant
-low anatomic dead space
what factors decrease FA/FI
decrease uptake:
-low solubility
-low cardiac output
what are determinants of tissue distribution
tissue blood flow
solubility of anesthetic in tissue
arterial blood to tissue gradient
what does the VRG include
heart, brain, kidney, liver, and endocrine glands
represents 10% of body mass
receives 75% of cardiac output
1st group to saturate with anesthetic gas
what is responsible for the majority of anesthesia continued uptake after VRG is saturated?
the muscle group
then fat once muscle is saturated
what are the ways volatile agents are eliminated
- ventilation
- hepatic biotransformation
-des 0.02%
-iso 0.2%
-sevo 2-5%
define FI
concentration gradient that pushes anesthetic agent from the vaporizer towards the alveoli
define FA
The anesthetic washes into the alveoli and establishes a partial pressure
what is uptake
the buildup of anesthetic partial pressure inside the alveoli is being opposed by continuous uptake of the agent into the blood
FA/FI curve for inhaled anesthetics
what metabolites are produced from des halothane and iso
trifluoroacetic acid (TFA)
small risk of immune mediated hepatic dysfunction
what metabolites are produced from sevo
free fluoride ions
theoretical risk of high output kidney failure
what are signs of high output renal failure
polyuria
hypernatremia
hyperosmolarity
increased plasma creatinine
inability to concentrate urine
what accelerates the production of compound A
desiccated soda lime
that is the recommended gas flow for sevo
1L/min for up to 2 MAC hrs
2L/min after 2 MAC-hrs
<1L/min not recommended at anytime
what is a MAC-hr
one times the minimum alveolar concentration that prevents movement in response to a noxious stimulus in 50% of subjects (MAC) administered for 1 hour
which P450 enzyme is chiefly responsible for halogenated anesthetic metabolism in the liver
CYP2E1
what by product of halothan metabolism has been implicated in causing halothane hepatitis
TFA
trifluoroacetic acid
concentration effect
the higher the concentration of inhalation anesthetic delivered to the alveolus (FA) the faster its onset of action (aka overpressuring)
what are the two components of the concentration affect
concentrating affect
augmented gas inflow effect
what is the concentrating effect
alveolus shrinks reducing the alveolar volume and causes relative increase in FA
what is augmented gas inflow effect
the concentrating effect causes an increased inflow of tracheal gas containing the anesthetic agent to replace the lost alveolar volume
this increase in alveolar ventilation augments FA
alveolar volume is restore quickly, so very temporary phenomenon
how does the concentration effect affect the rate of rise on the FA/FI curve
the higher the concentration of inhalation anesthetic delivered to the alveolus, the faster its onset of action
which concept best explains why N2O has faster onset than desflurane
concentrating effect
what is the ventilation effect
changes in alveolar ventilation affect the rate of rise in FA/FI
what is second gas effect
describes the consequences of the concentration effect when a second gas is co-administered with N2O
does the second gas effect have a more meaningful impact on iso or sevo and why
it produces more meaningful benefit with agents of higher blood: gas solubility
iso>sevo>des
what is the best way to mitigate diffusion hypoxia after N2O is discontinued
increase the FiO2 for 3-5 min after d/c N2O
it does not have to be 100% FiO2
how does right to left shunt affect FA/FI
slower induction with volatile agent (less soluble agents are affected to a greater extent)
faster induction with an IV agent
how does left to right shunt affect FA/FI
no meaningful impact on induction with a volatile agent
slower induction with an IV agent
what is the MAC value for iso
1.15
what is the MAC value for sevo
2.10
what is the MAC value for des
7.25
what is the process of converting liquids/solids to vapor
vaporization
what is the temperature of a liquid at which point the majority will be converted to vapor
boiling point
what determines the rate of vaporization
temp
vapor pressure of liquid
partial pressure of the vapor above the evaporating liquid
what is gas molecules exerting kinetic energy as a pressure measured in mmHg
vapor pressure
vapor pressure is dependent only on
temp
as temp increased, vapor pressure
increases
what is the vapor pressure of isoflurane
238 mmHg
what is the vapor pressure of sevo
160 mmhg
what is the vapor pressure of des
660 mmhg
all liquids that exert high vapor pressure are known as a
volatile liquid
if des is placed in an iso vaporizer, concentration will be -________ than expected
higher
if iso is placed in a des vaporizer, the concentration will be _________ than expected
less
what is the MAC vol% of Iso
1.15
what is the MAC vol% of Sevo
2.10
what is the MAC vol % of Des
7.25
what is the Pmac1 of iso at atmosphere
8.7 mmHg
what is the partial pressure of sevo at atmosphere
16
what is the Pmac1 of Des at atmosphere
55
what is the constant in charles law
pressure
what are the variables in the charles law
temp
volume
according to charles law as temp increases, volume _______________
increases
what is henrys law
at a constant temperature, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas at equilibrium above the gas-liquid interfaces
what is the solubility constant for O2
0.003ml/100ml
what is the constant for CO2
0.067 ml/100ml
what is grahams law
the rate of effusion of a gas is inversely proportional to the square root of its molecular weight
(the bigger the molecule the slower)
what is 1 MAC
the amount of gas where 50% of patients do not move under surgical stimulation
what is MAC based on
sea level,
no other sedatives/narcotics,
40 yo male
what factors increase MAC (meaning you need more gas)
-hyperthermia (henrys law)
-alcohol abuse
-drug-induced central nervous system activity (MAOIs)
-Hypernatremia
-age <40
what factors decrease MAC (so you need less gas)
hypothermia
age over 40
A2 agonists
acute alcohol ingestion
sedatives narcotics
factors increase MAC
hyperthermia
drug induced increases in central nervous system activity
hypernatremia
chronic alcohol abuse
factors decrease MAC (from naglehaut)
-hypothermia
-increasing age
-preopsedatives
-drug-induced decreases in central nervous system activities
-alpha2 agonists
-acute alcohol ingestion
-pregnancy
-postpartum
-lithium
-lidocaine
-hypoxia
-hypotension
-cardiopulmonary bypass
-hyponatremia
what does blood gas partition coefficient tell us
speed of uptake and elimination
the lower the blood gas coefficient the ________ the onset/offset
faster
blood gas partition tells you how much gas in is _______ as compared to tissues
blood
the _______ the blood solubility the slower the uptake to the brain, so the slower the onset/elimination
higher
what is the BG coefficient of ISO
1.4
what is the BG coefficient of SEVO
0.6
what is the BG coefficient of DES
0.42
what is the BG coefficient of N2O
0.47
what is the fastest gas in practice
N2O
what does a BG coefficient of 1.4 mean
1.4x as much drug stay in blood rather than the tissue
blood gas partition coefficients
how does an MV affect onset/offset of gases
increased MV increases onset/offset
what order of tissues do inhaled gases enter
vessel rich to vessel poor
Muscle>Fat>cartilage>bone
what is the concentration affect
filling the breathing tube with gas to give a “loading dose” of gas
what type of gas works best with concentration effect
higher BG coefficients like iso
how does concentration effect affect onset
increase speed of onset
when do we usually use concentration effect
with kids (ear tubes, tonsillectomy)
what is the second gas effect
volatile + N2O speeds onset or emergence
N2O acts a a carrier
what happens with second gas effect and emergence
N2O brings gas back into lungs causing a dilutional hypoxia (decreased O2 in alveoli)
how does the addition of N20 affect the concentration of other gases
increases concentration
N20 is _____x more soluble than nitrogen
34
how do you correct dilutional hypoxia
give 100% O2
What does the oil:gas partition coefficient correlate with
potency
what agent was oil/gas coefficient tested in
olive oil
the higher the oil:gas coefficient, the ________ the potentency
higher
the higher the oil:gas coefficient the _________ agent able to penetrate the BBB
more
a gas with _______ MAC # has more potency
lower
oil: gas coefficiency is like
lipid solubility
the higher the oil:gas the _______- the MAC
lower
MAC/ BG/ OG coefficients
what is the MAC % of SEVO
2
what is the BGC of SEVO
0.6
what is the OGC of SEVO
50
what is the MAC % of ISO
1.15
what is the BGC of ISO
1.4
what is the OGC of ISO
99
what is the MAC% of N2O
105
what is the BGC of N2O
0.47
what is the OGC of N2O
1.4
what is the BGC of DES
0.42
what is the OGC of DES
18.7
what is stage one of anesthesia
analgesia
mild cortical center depression
loss of sensation to pain
skeletal muscle movement intact
T/F we often see stage 1 anesthesia
F, usually skip straight to 3
what is stage two of anesthesia
excitement
central depression of motor centers, involuntary system is dominant
urinary incontinence
tachy
htn
tachypnea
eyes divergent
T/F we extubate in stage 2
false
T/F we should stimulate patients in stage 2
false
do not stimulate
what is stage 3 anesthesia
surgical anesthesia
what is stage 4 anesthesia
OD, dead, resp paralysis, severe CV/resp depression
what is stage 3 plane 1
loss of spinal reflexes (spontaneous breathing)
what is stage 3 plane 2
decreased muscle reflexes
what is stage 3 plane 3
paralysis of intercostal muscles (true deep sx anesthesia)
what is stage 3 plane 4
loss of muscle tone
decreased BP, dont want to be here
vaporizer delivery output calculation
what is the volume of breathing circuit
8L
what is Fa
alveolar gas concentration
what is an indicator of brain concentration
FA
what process allows gas to move from blood to tissues
simple diffusion
1 time constant is equal to what percentage
63%
2 time constants is equal to what percentage
86%
3 time constants is equal to what percentage
95%
4 time constants is equal to what percentage
98%
what is the formula for time constant
T= volume of circuit (8L) / fresh gas flow
if fresh gas flow is 2L/min what is your time constant
4 min
what is Fi
Concentration of anesthetic exiting the vaporizer
what factors affect Fa/Fi fraction
Fi
inspired concentration
fresh gas flow
circuit volume
dead space
mv
FRC
Fa
solubility
CO
partial pressures
what causes an increase in Fa/Fi
low solubility
low CO
high fresh gas flows
high MV
what causes a decreased Fa/Fi
high solubility
high CO
low fresh gas flows
low MV
What anesthetics are ethers
Des
Iso
Sevo
Enflurane
Methoxyflurane
Ether
What anesthetics are alkanes
Halothane
Chloroform
What anesthetics are gases
Nitrous oxide
Cyclopropane
Xenon
IUPAC name for desflurane
Difluoromethyl 1,2,2,2-tetrafluoroethyl ether
IUPAC name for sevo
Fluoromethyl 2,2,2-trifluoro-1-(trifluoromethyl) Ethyl ether
IUPAC name for iso
1-Chloro 2,2,2-trifluoroethyl difluoromethyl ether
IUPAC name for halothane
2-bromo-2-chloro-1,1,1-trifluoroethane
What’s another term for pseudocholinesterase
Butyrylcholinesterase
What are the steroidal NDNMB
Roc
Vec
Pancuronium
what is this
sevoflurane
what is this
desflurane
what is this
isoflurane
what is this
halothane
what is this
nitrous oxide
high vapor pressure agent in a low vapor pressure agent vaporizer would result in
higher concentration than desired
vapor pressure is solely dependent on
temp
standard conditions
760 atm
760 mmHg
29.92 inch pressure
Higher blood solubility =
Slower uptake to the brain
Slower onset and elimination
Blood: gas represents
Onset
Oil :gas represents
Potency
Thiopental induction dose
3-6 mg/kg
Thiopental sedation dose
0.5-1.5mg/kg
Thiopental DOA
5-8 min
Thiopental 1/2 life
11 hrs
Drug chloride is a weak
Base
Weak acid drugs have what in the name
Na Mg or Ca
