Volatile - Concepts Flashcards
Concentration that will produce absence of movement in 99% of people in response to a noxious stimulus
1.3 MAC
B:G N2O
0.46
B:G desflurane
0.42
B:G sevoflurane
0.69
B:G Isoflurane
1.4
B:G enflurane
1.8
B:G halothane
2.4
B:G Diethyl ether
12
lower hematocrit will alter
the B:G coefficient
With a HCT of 21 (vs 43)
the B:G coefficient will be 20% less.
Effectively having a LOWER solubility and therefore increased induction
the faster FA = FI
the faster the onset
PAlveoli is used to estimate
aka Fa is used to estimate
depth of anesthesia
recovery from anesthesia
anesthesia potency or MAC
PAlveoli is determined by (4)
- Pi
- Alveolar ventilation
- Breathing Circuit
- FRC
The higher the alveolar ventilation
the faster the onset
first knee of Fa/Fi =
saturation of vessel rich group
second knee of Fa/Fi =
saturation of muscle group
terminal climb after second knee of Fa/Fi =
progressing to saturation of vessel poor group, i.e. fat. Would take a very long amount of time
terminal climb after second knee of Fa/Fi =
progressing to saturation of vessel poor group, i.e. fat. Would take a very long amount of time
uptake of a volatile agent is determined by
- solubility of agent
- cardiac output
- A-v [alveolar to venous] pressure differences
The higher the FRC
the SLOWER the induction
induction is faster in
children , smaller FRC
To achieve faster induction with agents that are more soluble
we over pressure.
high initial input (Fi) offsets impact (duration) of uptake
Increased Cardiac output =
INCREASED uptake, effect of increasing solubility, net = slower induction
Decreased CO =
decreased uptake, effect of decreasing solubility = faster induction
Pulmonary blood flow =
CO
Agents more affected by CO are
soluble agents
vessel rich group reach equilibrium within
5-15 minutes
after induction, the FI should be decreased as
the VRG equilibrates and again as the MRG equilibrates
For maintenance, due to decrease in uptake over time
the FI should be decreased otherwise overdose
increasing ventilation is a more effective strategy with
a more soluble agent , doesn’t make much of a difference for lower solubility drugs
negative feedback in the spontaneously breathing ventilating patient
in spontaneously ventilating patient, as the % inspired increase, ventilation is depressed (r/t drug effect) and the Fa/Fi will decrease (r/t decrease in alveolar ventilation)
this is protective against overdose
if you keep someone spontaneously breathing on volatile agents, the risk for overdose is
low
larger circuit volume will decrease
FA/FI slope will decrease , overcome with higher flow rates
with conditions of higher metabolism, you may have
increased minute ventilation and also increased cardiac output . This results in net Fa/Fi increase but only slightly
right to left shunt is more consequential for
agents with LOW solubility
V/Q mismatches will
generally SLOW induction, more pronounced in less soluble agents
the concentration effect states that the higher the PI
the more quickly the PA will approach the PI
N2O to nitrogen
N2O is 34x more soluble
blood gas solubility of nitrogen
b:g 0.014
emergency and recovery depends on [4]
- length of anesthesia
- depth of anesthesia
- solubility of the agent
- MAC awake
sevoflurane’s biotransformation does result in
inorganic fluoride ions. Theoretical risk for fluoride induced high output renal failure.
[[unresponsive to ADH]]
Soda lime + sevo =
compound A
accelerated when desiccated
N2O irreversibly binds to
B12, which inhibits methionine synthase and thymidylate synthesis
potential effects of prolonged exposure to N2O and B12
megaloblastic anemia [bone marrow suppression] neuropathy immunocompromise impaired DNA synthesis concern for teratogenicity? possible spontaneous abortion homocysteine accumulation
previous history of alcoholism, pernicious anemia, strict vegan diet make these more likely
amnesia and loss of consciousness occur at
LOWER MACs also these are SUPRASPINAL
MAC awake =
alveolar concentration at which a patient opens his or her eyes,
MAC bar =
alveolar concentration at which autonomic responses are blunted (1.5 MAC)
HYPONATREMIA and MAC
hyponatremia will decrease MAC
Older age and MAC
6% reduction in MAC for every decade after 40
Hyperkalemia and MAC
no effect on MAC -
hyperkalemia, hypokalemia
hypermagnesemia, hypomagnesemia
Hyperthermia and MAC
MAC will INCREASE.
Hypothermia and MAC
MAC will DECREASE
In red heads, MAC is generally
increased by 19%
“presumably due to mutations in the melanocyte stimulating hormone receptor and an increased production of pheomelanin”
Meyer-Overton Rule
Meyer-overton rule states that lipid solubility is directly proportional to the potency of an inhaled anesthetic .
or, the greater the lipid solubility the lower the MAC value. [the greater the potency]
Implies the depth of anesthesia is determined by the number of anesthetic molecules that are dissolved in the brain and not necessarily the particular anesthetic agent that is used.
unitary hypothesis
states that all anesthetics share a similar mechanism of action, but each may work at a different site.
General rule, volatile anesthetics have the following effects on their target receptors
stimulate inhibitory pathways [GABA, GLYCINE, K channels]
Inhibit stimulatory pathways [NMDA, Nicotinic, sodium, dendritic spine function and motility ]
In the brain, the most important site of volatile anesthetic action is the
GABA A receptor
spine -> glycine receptor
NMDA receptor
Na+ channel inhibition.
Immobility is not due to GABA a in the spinal cord
ventral horn of spinal cord, glycine
N2O + opioid =
can cause myocardial depression
current theory on anesthetics
current potential sites of actions are modulating proteins:
- pre-synaptic voltaged gated sodium channels
- 2-pore potassium channels [trek + task}
- Inotropic and metabotropic receptors
either inhibit stimulatory or stimulate inhibitory
stage 1 of anesthesia
“analgesia or induction stage”
dizziness, a sense of unreality, and lessening sensitivity to touch and pain
Sense of hearing is INCREASED and responses to noises are INTENSIFIED
stage 2 of anesthesia
is the stage of excitement. Vital signs show evidence of physiological stimulation, pt may respond violently to very little stimulation, MOST susceptible to laryngospasm
stage 3 of anesthesia
Surgical anesthesia! Here we have 4 plans.
Each successive plane is achieved by increasing the concentrations of the anesthetic agent
stage 4 of anesthesia
OVERDOSE! toxic or danger stage.
fourth plane of anesthesia
demonstrated by cardiovascular impairment that results fro diaphragmatic paralysis, if this plane is not corrected immediately, stage 4 quickly ensues
thymol is used in
Halothane as a preservative. Can cause sticky turnstiles or temperature compensating valves
risk factors for halothane hepatitis
obese, female, multiple exposures to halothane
classic presentation of halothane hepatitis
fever, anorexia, nausea, chills ,myalgia, rash, arthralgia, eosinophilia followed by jaundice 3-6 days later
volatile not recommended during cardiac ablation
ISOFLURANE
it increases the refractoriness of accessory pathways and AV conduction so can interfere with interpretation of electrophysiological studies
Isoflurane decrease in BP is because of
decrease in SVR
CO in isoflurane is
maintained by HR, because partial preservation of baroreceptors
tachypnea less pronounced at 1 MAC with
isoflurane
electrically silent EEG at 2MAC with
isoflurane
vasodilator of hepatic circulation
isoflurane
isoflurane C/i
MH or maybe* extremely low CO -> r/t decrease in SVR
Desflurane baroreceptors
INTACT
isoflurane baroreceptors
partial preservation
Decrease BP with desflurane is r/t
Decreased SVR
When you give a higher concentration of desflurane [overpressure]
you will have a sympathomimetic effect, rapid transient increase in transient HR, blood pressure, catecholamine levels,
desflurane C/I
malignant hyperthermia
kind of asthmatics
CO not as well maintained with
sevoflurane
Only common agent that does not increase R atrial pressure / CVP
sevoflurane
best choice of a volatile for asthmatics is
sevoflurane because minimal airway irritation
hepatic blood flow with sevo
is maintained
sevoflurane C/I
MH and relative: renal impairment
enflurane and hypoxic drive
ABOLISHED. Marked respiratory depression at 1 MAC
Depresses mucociliary function
enflurance
Increased secretion of CSF but decreased outflow
Enflurane
EEG changes with enflurane are exacerbated by
high concentrations, hypocapnia, and repetitive auditory stim
Hyperventilation with enflurane
IS NOT RECOMMENDED, can exacerbate EEG changes and lead to seizures
enflurane C/I
avoid in patients with pre-existing kidney disease or impairment
avoid in patients with known or suspected seizure disorder
avoid in patients with increased ICP
MH
OSHA and waste gas
no worked should be exposed to more than
2 ppm halogenated agents in o2
0.55 halogenated if used with n2o
25 ppm n2O
no significant increase in MAC until
> 1.5 MAC
increase risk of arrthymias with epi
Halothane
enflurane
N2O
aminophylline is linked to serious
ventricular dysrthymias when used with halothane
most potent MH trigger
halothane
things that increase MAC (6)
1. chronic ETOH 2 .Increased CNS neurotransmitters 3. HYPERnatremia 4. Increased in infants 1 -6 months 5. HYPERthermia 6. Red hair
factors that decrease MAC (16)
- acute ETOH
- IV anesthetics
- N2O
- Opioids
- HYPONATREMIA
- Older age
- Prematurity
- HYPOthermia
- HYPOtensino
- HYPOxia
- Anemia
- Cardipulmonary by pass
- Metabolic Acidosis
- HYPOosmolarity
- Pregnancy through 72 hours post party
- PaCO2 >95 mmHg
