Inhaled Anesthetics Flashcards
describe 6 factors affecting equilibration (onset) times of inhaled anesthetics
distribution (Fa=Fi)
lung uptake
tissue uptake
solubility
cardiac output
arterio-venous concentration gradient
define potency (MAC) of inhaled anesthetics
equilibrium concentration required to prevent movement to skin incision at 1 ATM in 50% of px
list 3 factors that increase MAC requirements
hyperthermia
elevated CNS catecholamine NT release (anxiety)
chronic alcoholism
acute amphetamine use
hypernatremia
list 3 factors that decrease MAC requirements
hypothermia
pregnancy
shock
increasing age
acute alcohol ingestion
CNS depressant drugs
chronic amphetamine use
describe the probable mechanism of inhaled anesthetic action
ligand-gated ion channels are the most likely target
describe clinical effects of inhaled anesthetics on organ systems other than the CNS
decreased BP
decreased myocardial function
increased HR
decreased O2 consumption by muscles
faster respiratory rate
lower tidal volume of breath
when does equilibrium occur? what is the tissue conc at equilibrium?
when alveolar concentrations equal inspired concentrations (what is breathed in is what is breathed out - takes many hours, usually do not reach it)
max conc exists in the tissues
determinants of rate of rise of lung concentrations
inspired gas partial pressure
ventilation rate
functional residual capacity (FRC)
what happens when there is an increase in the inspired anesthetic concentration? What law is this?
increased rate of induction by increasing the rate of transfer into the blood
Fick’s law: flux = (C1-C2) x (area x permeability / thickness) - concentration gradient is proportional to diffusion across a membrane, which is inversely related to the thickness of the membrane
minute alveolar ventilation is another word for
ventilation rate
how does functional residual capacity affect induction time of inhaled anesthesia?
increased FRC slows the flow of agent into the lung, so induction time is increased (slowed)
why does increased FRC increase the induction time?
the increased volume of lung that must be filled to obtain the effect
although Fa rises by inspired conc, MAV, and FRC, the rise of concentration is slowed greatly by…
LARGE amount of TISSUE UPTAKE (including blood)
3 primary determinants of tissue uptake
solubility of the agent
pulmonary blood flow (i.e. cardiac output)
arterio-venous concentration gradient (in the lung)
a ratio that describes the solubility of an agent in the body
blood/gas partition coefficient (B/G)
a larger B/G partition coefficient…
increases blood uptake and decreases alveolar concentration, which SLOWS induction (due to greater tissue uptake)
problems associated with more soluble agents dissolving easily in the blood
increased equilibration times
reduced ability to exit the blood (blood holds the agent)
reduced ability to enter the brain and other tissues
halothane has a higher partition coefficient, so its induction time…
is slower than other drugs with lower B/G, and its slower to come off of
describe pulmonary outflow (cardiac output) as it pertains to equilibration time
increases in cardiac output DECREASES rate of alveolar concentration rise, and SLOWS equilibration time
clinical importance of cardiac output in an ER situation
low cardiac output of a victim combined with low blood volume could give tragic effects of regular anesthesia dose, due to preferential blood shunting to the brain!
as cardiac output increases, induction time..
increases (is slowed)
increased tissue uptake effect on blood concentrations
decreases blood concentrations, which increases blood uptake from the lungs
increased solubility of an agent
increased CO
increased AV conc gradient
ALL have what effect on equilibration time?
increase equilibration time (slow induction)
ligand-gated ion channel examples that are the most likely targets of MOA of inhaled anesthetics
nicotinic ACh recpetors
5HT receptors
amino acid receptors esp GABA
most prevalent transmitter in mammal CNS
GABA - inhibitory function in central coordination of excitability, motor, and autonomic activity
what happens at the GABA receptor when GABA binds?
Cl- influx, membrane hyperpolarizes, neuronal excitability is reduced
how do drugs enhanve GABAa current?
increasing Cl- influx, channel open frequency, and channel open duration
where do inhaled anesthetics bind to GABA receptors? So, are they agonists or antagonists?
bind at sites distinct from GABA binding sites, so they are GABA agonists
problems with GABA theories
GABAa activity is inhibited at high anesthetic conc
other GABAa agonists give anxiolysis (inhaled agents do not)
GABAa ANtagonists have little effect on inhaled agents
effect of hyper/hypo thyroidism on MAC
no effect
inhaled anesthetics effect on renal blood flow, glomerular filtration rate, hepatic blood flow, uterine smooth muscle,
decreased consistently
effect of N2O on nausea and vomiting
increased
what affects potency?
disease state, other meds, etc
list of inhaled anesthetics
desflurane
sevoflurane
isoflurane
halothane
nitrous oxide
