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225 Cards in this Set

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pharmacokinetics
absorption, distribution, metabolism, and excretion of inhaled or injected drugs; what the body does to the drug
pharmacodynamics
responsiveness of receptors to drugs & mechanism by which these effects occur; what the drug does to the body
receptors
components of cell that interacts w/ drugs to start a series of events leading to pharmacologic effects
what part of cell deals with the selectivity of drug action?
receptors
what terminates drug effects?
metabolism, excretion and/or redistribution to inactive sites
drugs interacting with other biologic components in a
geometrically specific way
stereoselective or stereospecific
enantiomers
2 substances of opposite shape
racemic mixture
2 enantiomers present in equal proportions (50:50)
are enantiomers in a racemic considered pharmacologically as the same or different drug?
different pharmacologically
the INACTIVE enantiomer in a racemic mixture is known as a(n) ________?
impurity
what part of a racemic mixture contributes to side effects?
inactive enantiomer (impurity)
clincally what fraction of drugs are admin as racemic mixures?
(ex. thiopental, ketamine, bupivacaine, volatiles)
1/3
agonists
drugs that activate receptors
antagonists
drugs that bind to receptors w/out activating them, preventing agonists from stimulating them
competitive antagonism(ex. NMBAs & Ach)
increasing concentrations of an antagonist progressively inhibit responses to unchanging concentrations of an agonists
noncompetitive antagonism
high concentrations of an agonist cannot completely overcome antagonism
additive effect
(Example: 2 inhaled anesthetics)
two drugs produce an effect equal to algebraic summation
synergistic effect
(Example: aminoglycoside & NMBAs)
two drugs produce an effect more than equal to algebraic summation
hyperreactive individuals
usual doses of drugs prodced increased effects
hyporeactive individuals
usual doses of drugs produce decreased effects
tolerance
hyporeactivity from chronic exposure to a drug
cross-tolerance
(ex. Inhaled anesthetics & chronic alcohol ingestion).
develops b/t drugs of different classes that produce similar pharmacolgic effects
tachyphylaxis
(ex. ephedrine)
tolerance that develops acutely with only a few doses of a drug
idiosyncrasy

what do they typically reflect?
unusual effect of a drug in uniquely susceptible pts regardless of the dose

mostly due to hypersensitivity (allergy)or genetic differences
dose-response curve
shows relationship b/t dose/plasma concentration of the drug and the resulting pharmacologic effects
what are the components of the dose response curve?
potency
slope
efficacy
individual responses
effective dose (ED)
doses required to produce a specific effect
ED50

ED90
doses required to produce a specific effect in 50% of pts

doses required to produce a specific effect in 90% of pts

etc.
what shifts the dose-response curve to the left?
increased affinity of a drug for its receptors
when calculating drugs by body wt, when will total body weight overestimate lean body mass?
when body wt > ideal body wt
at what adult wt for female and male is it rarely necessary to scale dose to body weight?
females > 80 kg
males > 100 kg
what influences the slope on the dose-response curve?
the number of receptors that must be occupied before a drug effect occurs
what dose a steep dose-response curve represent?
(ex. NMBA, inhaled agents)
a drug must occupy a majority of the receptors before effect occurs
when the dose-response curve is steep, small increases in doses will have what impact?
large increases in drug effect
what happents to the drug effect when you increase the MAC of a volatile from 1 to 1.3?
A 1 MAC concentration of a volatile anesthetic prevents skeletal muscle movement in response to surgical skin incision in 50% (ED50) of patients, whereas a further modest increase to about 1.3 MAC prevents movement in at lease 95% (ED95) of patients!
what is negative about drugs with steep dose-response curves? what does this mean in terms of volatile agents?
difference b/t therapeutic & toxic concentraions may be small

small difference b/t doses that produce desirable degrees of CNS depression & undesirable cardiopulmonary depression
efficacy
maximal effect of a drug
on what part of the dose-reponse curve is efficacy represented?
plateau
what can limit dosages of drugs below concentrations associated w/ its maximal effect?
undesirable side effects
are efficacy and potency of drugs always related?
no
what 2 pharmacological principles impact individual responses to drugs. Give examples of each.
1.pharmacokinetics
a.renal fxn
b.liver fxn
c.cardac fxn
d.age

and/or

2.pharmacodynamics
a.enzyme activity
b.genetic differences
pharmacokinetics of IV drugs is influenced by what 2 factors?
1. volume of distribution (Vd)
2.clearance
elimination half-time
rate at which plasma concentration of a durg decreases with time
what 2 factors determine elimination half-time?
1.volume of distribution (Vd)
2. clearance
what 2 things are more useful than elimination half-time in characterizing clinical responses to drugs?
1.context-sensitivity half-time
2.effect-site equilibrium time
volume of distribution (Vd)
dose of drug admin IV divided by plasma concentration
what does volume of distribution reflect?
the apparent volumes of the bodies compartments (of the compartment model) for that drug
what 3 drug properties limit passage of drugs into tissues resulting in a small Vd?
1.binding to plasma protein
2.high degree of ionization
3.low lipid solubility
are the tissues peripheral or central compartments?
peripheral
do NMBAs have small or large Vd? why?
small Vd

b/c they are more ionized and stay in the ECF
is the body's circulation considered a peripheral or central compartment?
central
are the plasma concentrations of nonionized lipid solubles drugs high or low? why?
low

b/c they easily pass into tissue from the circulation
are nonionized drugs lipid or water soluble?
(ex. thiopental, diazepam)
lipid soluble
do nonionized drugs have large or small Vds? why?
large

b/c they are lipid soluble
Are volume of distributions representations of absolute anatomic volumes?
No
Clearance
Volume of plasma (central compartment) cleared of drug by renal excretion and/or metabolism in liver or other organs
What are the units for clearance?
ml/min
What is one of the most important pharmacokinetic variables to consider when defining a constant rate of IV drug infusion?
Clearance
When the rate of a drug infusion > clearance what 2 things happen?
1.plasma concentration increase more
2.cumulative drug effects occur
Which organ is the most important organ for clearance of unchanged drugs or their metabolites?
Kidneys
Which compounds are excreted more efficiently? Water soluble compounds not bound to proteins or lipid soluble protein-bound drugs
Water soluble compounds not bound to proteins
What 2 clinical lab indicators are useful for assessing the ability of kidneys for eliminate drugs?
1.creatinine clearance
2.serum creatinine concentrations
What benefit do creatinine clearance and serum creatinine concentrations have for drugs dosing?
Provides an estimate for downward adjustments of drug dosages to prevent accumulation of drug in plasma
What is the primary organ for metabolism?
Liver
What are 3 secondary organs for metabolism?
1.kidneys
2.lungs
3.GI tract
For water soluble drugs, are the following increased or decreased?
A.Vd
B.renal excretion
A.Vd = decreased
B.renal excretion = increased
For lipid soluble drugs, are the following increased or decreased?
A.Vd
B.renal excretion
A.Vd = increased
B.renal excretion = decreased
Why is renal excretion of lipid soluble compounds decreased? Hint: thing about kidney sites & mechanisms
Excretion is decreased b/c of ease of reabsorption from lumens of renal tubules into pericapillary fluid
What enzymes participate in metabolism of many drugs? And where are they located?
Microsomal enzymes

liver
What specific site of the liver are microsomal enzymes?
Hepatic smooth endoplasmic reticulum
What were microsomal enzymes derived from?
centrifuged homogenized hepatocytes from disrupted smooth endoplasmic reticulum know as microsomal fraction containing the cytochrome P450 system
What is the plasma concentration curve?
A graphic plot of the logarithm of the plasma concentration of drug vs time following rapid IV (bolus) injection
How many phases does the plasma concentration curve have? And what are they?
2

1.Distribution (alpha) phase & 2.elimination (beta) phase
What do the two plasma concentration curve phases characterize?
Distribution half-time of the drug
What does first phase distribution (alpha) phase correspond with?
The initial distribution of drug from circulation to tissues
What does second phase elimination (beta) phase correspond with?
Gradual elimination in plasma concentration of drug from central vascular compartment by renal and hepatic mechanisms
Elimination half-time
Time needed for plasma concentration of drug to decreased 50% during elimination phase
How many elimination half-times are needed for almost complete elimination of a drug?
5
What does dose intervals more frequent than 5 elimination half-times result in? (2)
1.Accumulation of the drug
2.Cumulative drug effects
How many elimination half-times does it take for a drug to achieve steady state plasma concentration (Cps) with intermittent doses?
5 elimination half-times
Which compartment model is elimination half-time more useful?
One-compartment model (central compartment)
Elimination half-time shows virtually no insight into rate of decrease in plasma concentration after dc of ___________.
IV drug administration
Context-sensitive half-time
Time needed for drug concentration to decrease a predetermined percentage after dc of continuous IV infusion of a specific duration
Context of context-sensitive half-time refers to?
Duration of infusion
What 3 things does context-sensitive half-time largely depend on?
1.drug lipid solubility
2.efficiency of drug clearance mechanisms
3.duration of continuous IV admin
What happens to context-sensitive half-time when duration of continuous IV administration increases?
Increases
is context-sensitive half-time related to elimination half-time of a drug?
No
In relation to drugs, what does time to recovery depend on?
How far plasma concentration must decrease to reach levels compatible with awakening
If concentration of drug admin by continuous infusion is just above that needed to awaken, is time to recover slow or rapid?
Rapid
If concentration of drug admin by continuous infusion is much higher than that needed to awaken, is time to recover slow or rapid?
Slow
What does BIS stand for?
Bispectral Index
Why is the BIS beneficial in regard to IV drugs?
Allows more precise titration for more desired level of drug effect
Effect-Site Equilibration time
is time for equilibration between drug concentration in plasma and drug effect
What’s a clinical benefit of effect-site equilibration times?
Logical timing of IV drug admin (dosing intervals)
Drugs with short effect-site equilibration times will produce slow or rapid onset of pharmacologic effects?
(ex. remifentanil, alfentanil, thiopental, propofol)
Rapid
Drugs with longer effect-site equilibration times will produce slow or rapid onset of pharmacologic effects?
(ex. fentanl, sufentanil, midazolam)
Slow
Nonionized
– active and lipid soluble
Ionized
– inactive, and water soluble
Degree of ionization of drug is a function of what 2 things.
1.pK
2.pH of surrounding fluid
What does it mean when pK and pH are identical?
50% of drug exists in ionized form
if pH and pK values are similar small changes in pH can result in?
large changes in degree of ionization
What type of drugs are highly ionized at an alkaline pH ?
(ex. barbiturates)
Acidic drugs
What are highly ionized at an acid pH?
(ex. opioids, local anesthetics)
Basic drugs
Which route of administration of drugs ensures the best achievement of predictable plasma concentration?
IV
Is IM admin predictable or unpredictable? And what is it dependent on?
unpredictable

local blood flow
What is first-pass hepatic effect?
Drugs enter portal venous blood, passes through liver before entering systemic circulation
What is reason for large differences between effective oral and IV doses?
First-pass hepatic effect
What phenomenon effects GI (small intestine) admin?
First-pass hepatic effect
first-pass pulmonary effect
uptake of basic lipophilic amines (lidocaine, propranolol, fentanyl) into the lungs which serve as a reservoir to release drugs back into systemic circulation
Following systemic absorption, which tissues receive larger amount of total dose?
highly perfused tissues (brain, heart, kidneys, liver)
____% of CO is delivered to about _____% of total body mass.
75%; 10%
redistribution
As plasma concentration decreases below highly perfused tissues, drugs go to less perfused tissues (skeletal muscle)
What is principally responsible for awakening after single dose of a drug?
Redistribution
At the cellular level how do drugs exert pharmacologic effects?
by interacting with receptors
Receptors
Transmembrane protein molecules in the lipid
bilayer of the cell
Regarding the drug-receptor interaction, what initiates or prevents a series of changes that characterize the pharmacologic effects of the drug?
altered function or conformation of a specific cellular component
Name 3 excitable transmembrane protein receptors.
1.voltage-sensitive ion channels
2. Ligand-gated ion channels
3. Transmembrane receptors
Voltage-sensitive ion channels
ion channels that open and close depending on cell membrane voltage
What are some examples of voltage-sensitive ion channels?
Na, Cl, K, Ca
Ligand-gated ion channels
nicotinic cholinergic receptors & amino acid receptors (GABA) function as receptor-ion channel complexes
What does GABA stand for?
Gama-Aminobutyric Acid Receptor
Activation of GABA results in? (3)
1.cell hyperpolarization or an increase in ion conductance that prevents depolarization
2. inhibition of neuronal activity in the CNS
3.hypnotic and sedative effects
Give 3 examples of drugs that activate GABA
1.benzodiazepines
2.barbiturates
3.propofol
How many of the synapses in CNS are GABA receptors?
Approximately 1/3 of all synapses
Regarding the GABA receptor, what do Opioids and alpha-2 agonists do at the presynaptic site?
may inhibit the presynaptic calcium ion channels responsible for activating neurotransmitter release
What are G Proteins?
important intermediaries in cell communication; second messengers
What does G protein stand for?
Guanine Nucleotide Proteins
How does the mechanism of second messenger with G proteins work?
1.Exogenously administered drugs
2.recognized by specific receptor
3. receptor-ligand interaction
4.conformational change
5.specific G-protein activated
6.mediation of the final cascade of biological steps within the cell that lead to pharmacologic or physiologic response
7.effector site (enzyme) will be activated or inhibited or the ion channel may be opened or closed in response to G-protein.
Clinically important G Protein-coupled receptor systems? (6)
1.adrenergic (alpha-1, alpha-2, beta-1, beta-2)
2.opioid
3.muscarinic (mu-1, mu-2)
4.cholinergic
5.dopamine
6.histamine (H-1, H-2)
Name the chemical name for the 2 racemic mixture components.
the dextro (d) or levo (l) isomer
Are the number of receptors in the body static or dynamic?
Dynamic
Up-Regulation
increasing number of receptors in response to decreased stimulation
Down-Regulation
Decreasing number of receptors in response to increased stimulation
steady state conditions
plasma concentrations of drugs are proportional, or equal, to receptor concentration of drugs
concentration of drugs at receptors will be influence by what factors? (pharmacokinetics or pharmocodynamics)
Pharmacokinetic factors that influence plasma concentrations of drugs tissue uptake, renal excretion, hepatic metabolism)
Relationship between plasma concentration of drugs and pharmacologic response elicited is influenced by? (pharmacokinetics or pharmocodynamics)
Pharmacodynamics
Pharmacokinetics of inhaled anesthetics describes?
1.Uptake (absorption) from alveoli into systemic circulation
2.Distribution in the body
3.Elimination via lungs or metabolism (principally in liver)
Controlling the inspired partial pressure (PI) creates what?
a gradient so that the anesthetic is delivered from the anesthesia machine to the site of action
The primary objective of inhalation anesthesia?
achieve a constant & optimal brain partial pressure (Pbr) of the anesthetic
What is PI?
Inspired partial pressure
What’s Pbr?
Brain partial pressure
What’s Pa?
Arterial partial pressure
What’s PA?
Alveolar partial pressure
What mirrors Pbr of an inhaled anesthetic?
PA
What 3 things is PA able to determine?
1.index of anesthetic depth
2.rate of induction & recovery of anesthesia
3.measure of equal potency
What Factors Determine the Alveolar Partial Pressure?
input (delivery) into the alveoli minus uptake (loss) from alveoli into pulmonary arterial
Input of inhaled anesthetic is dependent on what 3 things?
1.Partial pressure inspired (PI)
2.Alveolar ventilation (VA)
3.Characteristics of anesthetic breathing system
Uptake of inhaled anesthetic is dependent on what 3 things?
1.Solubility
2.CO
3.Alveolar-to-venous partial pressure difference (A-vD)
Are metabolism & percutaneous loss of inhaled anesthetics a significant influence on PA during induction & maintenance of anesthesia?
No
What 3 factors determine partial pressure gradients necessary for establishment of anesthesia?
1.Transfer of inhaled anesthetic from anesthetic machine to alveoli

2.Transfer of inhaled anesthetic from alveoli to arterial blood

3.Transfer of inhaled anesthetic from arterial blood to brain
What 3 things influences transfer of inhaled anesthetic from anesthetic machine to alveoli?
a.Inspired partial pressure
b.Alveolar ventilation c.Characteristics of anesthetic breathing system
What 3 things influence transfer of inhaled anesthetic from alveoli to arterial blood ?
a.Blood:gas partition coefficient
b.CO
c.Alveolar-to-venous partial pressure difference
What 3 things influence transfer of inhaled anesthetic from arterial blood to brain ?
a.Brain:blood partition coefficient
b.Cerebral blood flow
c.Arterial-to-venous partial pressure difference
Concentration effect
-What is it?
-What does it inevitably do?
A high PI (input) is necessary during INITIAL administration of inhaled anesthetic to offset impact of uptake into blood, accelerating induction of anesthesia as reflected by rate of increase in the PA.
Why is decreasing PI after optimal PA level reached critical?
to match decreasing uptake & maintaining a constant and optimal Pbr
When will you decrease PI?
as uptake into blood decreases
Does the concentration effect and the second gas effect work dependently or independently?
Independently
second gas effect
ability of the large volume uptake of one gas (first gas) to accelerate the rate of increase of the PA of the co-administered gas (second gas)
alveolar hyperoxygenation
transient increase (about 10%) in Pao2 that accompanies early phase of nitrous oxide administration reflects second gas effect of nitrous oxide on oxygen
Increased VA, like PI, will do what to the inhaled anesthetic, PA, and induction time? And what will have the opposite effect?
promote input of inhaled anesthetics to offset uptake into the blood; more rapid rate of increase in PA and induction of anesthesia

hypoventilation
How does controlled ventilation of lungs accelerates rate of increase of the PA?
hyperventilation (increased VA) and decreased venous return(decreased CO)
Risk of anesthetic overdose may be increased during what type of ventilation?
controlled ventilation of lungs
What characteristics of the anesthetic breathing system influences rate of increased of PA?
1.Volume of the system
2.Solubility of inhaled anesthetics in the rubber or plastic components of the system
3.Gas inflow from the anesthesia machine
How is solubility of inhaled anesthetics in blood and tissues expressed?
partition coefficients
partition coefficients
distribution ratio describing how the inhaled anesthetic distributes itself between two phases at equilibrium (when partial pressures are identical)
What does it mean when Blood:gas partition coefficient is 10?
concentration of inhaled anesthetic is 10 in the blood and 1 in the alveolar gas when partial pressures of anesthetic in these two phases are identical
Partition coefficients are _________-dependent.
temperature
The solubility of a gas in a liquid is increased when the temperature of the liquid ___________.
decreased
partition coefficients are usually for what temperature, unless otherwised stated?
37ºC
What factor determines amount of inhaled anesthetic that must be dissolved (undergo uptake) in blood before equilibrium with gas phase is reached?
Solubility
Blood is considered a pharmacologically active or inactive reservoir?
pharmacologically inactive reservoir
the size of the resevoir provided by blood is determined by?
the solubility of the anesthetic in the blood
When blood:gas partition coefficient is ___ (high or low) a large amount of anesthetic must be dissolved in blood before the Pa = PA.
high
When blood:gas partition coefficient is ___ (high or low) minimal amounts of anesthetic have to be reached so that the rate of increase of the PA =Pa=Pbr are rapid.
low
Blood:Gas Partition Coefficients
time necessary for equilibration of PA with Pa
Tissue:Blood Partition Coefficients
time necessary for equilibration of Pa with tissue
What has to be calculated to predict tissue:blood partition coefficients?
time constant for each tissue
time constant
amount of inhaled anesthetic that can be dissolved in tissue divided by tissue blood flow
Complete equilibration of any tissue, including the brain, with the Pa requires at least how many time constants?
three time constants
for more soluble agents like halothane nad isoflurane, one time constant is equal to? so how long would it take for complete equilibrium with any tissue (e.g. brain)?
about 3-4 minutes

about 10-15 minutes
for less soluble agents like nitrous oxide, desflurane and sevoflurane, one time constant is equal to? so how long would it take for complete equilibrium with any tissue (e.g. brain)?
about 2 minutes

about 6 minutes
Blood:gas partition coefficient of nitrous oxide (0.46) is ____ times greater than that of nitrogen (0.014). What does this mean?
34

Means that Nitrous oxide can leave the blood to enter an air-filled cavity 34 times more rapidly than nitrogen can leave the cavity to enter the blood.
Entrance of nitrous oxide into an air-filled cavity surrounded by a ______ causes the gas space to expand. Give examples.
compliant wall (intestinal gas, pneumothorax, pulmonary blebs, air embolism)
Entrance of nitrous oxide into air-filled cavity by a _____ causes an increase in pressure. Give examples.
non compliant wall(middle ear, cerebral ventricles, supratentorial subdural space)
Magnitude of volume or pressure increase in air-fill cavity when administering nitrous oxide is influenced by what 3 things?
1.PA of nitrous oxide

2.Blood flow to air-filled cavity

3.Duration of nitrous oxide administration
Contraindications for nitrous oxide administration.
1.closed pneumothorax

2.trauma (rib fractures)

3.venous air embolism
How does high cardiac output influence rate of increase of PA and rate of anesthesia induction?
decreased rate of increased of PA & slow induction of anesthesia
How does slow cardiac output influence rate of increase of PA and rate of anesthesia induction?
increased rate of increased of PA & fast induction of anesthesia
What effect does a right-to-left intracardiac or intrapulmonary shunt have on rate of induction of anesthesia? Why?
slows rate of induction of anesthesia

dilutional effect
what effect does wasted ventilation (dead space) have on rate of induction of anesthesia? why?
no effect

no dilutional effect on Pa produced
what does Alveolar-to-Venous Partial Pressure Differences (A-vD)reflect?
tissue uptake of inhaled anesthetics
Skeletal muscle and fat represent about ___% of body mass, and receive less than ___% of CO.
70%; 25%
What tissues continue to act as inactive reservoirs for anesthetic uptake for several hours?
Tissues like skeletal muscle and fat
Is Equilibration of inhaled anesthetics between fat & arterial blood ever achieved?
probably never achieved
How can recovery from inhaled anesthesia be defined?
rate at which the PA decreases with time
how does recovery from anesthesia differs from induction of anesthesia ? (3)
1.Absence of a concentration effect on recovery (PI cannot be less than zero)

2.Variable tissue concentrations of anesthetics at start of recovery

3.Potential importance of metabolism on rate of decrease in the PA
Impact of tissue storage on recovery depends on? (2)
a.Duration of anesthesia

b. Solubility of anesthetic in various tissue compartments
Which agents have longest recovery more soluble or less soluble ones? Give examples.
more soluble

more solubles = halothane, isoflurane

poorly solubles = sevoflurane and desflurane
which volatile agent(s) is/are dependent on metabolism and VA for decrease in PA? why?
halothane

it's a highly lipid soluble methoxyflurane
which volatile agent(s) is/are dependent on VA for decrease in PA? why?
isoflurane, desflurane, and sevoflurane

less lipid soluble
Time needed for a 50% decrease in anesthetic concentration of isoflurane, desflurane and sevoflurane? and does it increase significantly with increased duration of anesthesia?
less than 5 minutes

no
when does the principle difference in rates at which desflurane, sevoflurane, and isoflurane are eliminated occur?
in the final 20% of the elimination process
a.When does diffusion hypoxia occur? b.How does diffusion hypoxia occur?
a.at conclusion of nitrous oxide administration if patients are allowed to inhale room air
b.initial high volume outpouring of nitrous oxide from blood into alveoli when inhalation of this gas is discontinued can so dilute the PAo2, that the Pao2 decreases.
how can diffusion hypoxia be prevented?
by filling patients lungs with oxygen at conclusion of nitrous oxide administration.
What does MAC stand for?
Minimum Alveolar Concentration
MAC
the minimum alveolar concentration (partial pressure) of an inhaled anesthetic at 1 atmosphere (atm) that prevents skeletal muscle movement in response to a noxious stimulus (surgical skin incision) in 50% of patients.
WHy is MAC the most useful index of anesthetic equal potency for comparison between inhaled anesthetics?
because MAC reflects the partial pressure at the anesthetic site of action (Pbr)
Are MAC values for combinations of inhaled anesthetics synergistic or additive?
additive
the MAC for volatile anesthetics is decreased about ___% for every ___% alveolar nitrous oxide concentration used.
1;1
give the reason for administering nitrous oxide with volatile anesthetics.
depression of ventilation and circulation is less when nitrous oxide is substituted for an equivalent MAC dose of volatile drug.
how much MAC required to prevent skeletal muscle movement in response to painful stimulation in nearly all patients during surgery?
1.3 MAC
Name some Physiologic and Pharmacologic Factors that have no impact on MAC. (8)
1.Duration of anesthesia
2.Gender
3.Anesthetic metabolism
4.Thyroid gland dysfunction
5.Hyperkalemia/Hypokalemia
6.Paco2 15-95mmHg
7.Pao2 >38
8.Spinal cord transaction/removal of forebrane in animals
Name some Physiologic and Pharmacologic Factors that increase MAC. (5)
1.Hyperthermia
2.Drugs that increase CNS catecholamines (MAOI’s, Tricyclic antidepressants, Cocaine, Acute amphetamine ingestion)
3.Infants
4.Hypernatremia
5.Chronic ethanol abuse
Name some Physiologic and Pharmacologic Factors that decrease MAC. (14)
1.Hypothermia
2.Preoperative medication
3.IV anesthetics
4.Neonates (as compared with infants)
5.Elderly
6.Pregnancy
7.Postpartum (return to normal in 20-72 hours)
8.Alpha-2 agonists
9.Lithium
10.Hyponatremia
11.Cardiopulmonary bypass
12.SBP <40 mmHg
13.Neuraxial opioids
14.Pao2 <38 mmHg
Lack of Skeletal muscle responses with inhaled anesthetic may be mediated where?
spinal cord
Amnesia responses of inhaled anesthetics may result from actions at?
supraspinal sites in a nonpolar environment
anesthetic drug-induced inhibition of synaptic transmission through what?
multineuronal polysynaptic pathways, especially the reticular activating system
what's the other name for Myer-Overton Theory?
(Critical-Volume Hypothesis)
What are the 2 principles of Myer-Overton Theory?
1.close correlation between lipid solubility of inhaled anesthetics (oil:gas partition coefficient) and their potencies (MAC).

2.anesthesia occurs when a sufficient number of anesthetic molecules dissolve (critical volume) in crucial hydrophobic sites, such as lipid cell membranes.
Isoflurance
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?
a. 1.46
b. 1.17
c. yes
Enflurane
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?
a. 1.9
b. 1.63
c. yes
Halothane
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?
a. 2.54
b. 0.75
c. no (Halothane hepatitis)
Desflurane
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?
a. 0.42
b. 6.6
c. yes
Sevoflurane
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?
a. 0.69
b. 1.8
c. no (Compound A, nephrotoxic)
Nitrous oxide (NO2)
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?
a. 0.46
b. 104
c. yes