Basics Of Anesthesia Chapter 2 Basic Pharmacologic Principles

Front 1

pharmacokinetics

Back 1

absorption, distribution, metabolism, and excretion of inhaled or injected drugs; what the body does to the drug

Front 2

pharmacodynamics

Back 2

responsiveness of receptors to drugs & mechanism by which these effects occur; what the drug does to the body

Front 3

receptors

Back 3

components of cell that interacts w/ drugs to start a series of events leading to pharmacologic effects

Front 4

what part of cell deals with the selectivity of drug action?

Back 4

receptors

Front 5

what terminates drug effects?

Back 5

metabolism, excretion and/or redistribution to inactive sites

Front 6

drugs interacting with other biologic components in a
geometrically specific way

Back 6

stereoselective or stereospecific

Front 7

enantiomers

Back 7

2 substances of opposite shape

Front 8

racemic mixture

Back 8

2 enantiomers present in equal proportions (50:50)

Front 9

are enantiomers in a racemic considered pharmacologically as the same or different drug?

Back 9

different pharmacologically

Front 10

the INACTIVE enantiomer in a racemic mixture is known as a(n) ________?

Back 10

impurity

Front 11

what part of a racemic mixture contributes to side effects?

Back 11

inactive enantiomer (impurity)

Front 12

clincally what fraction of drugs are admin as racemic mixures?
(ex. thiopental, ketamine, bupivacaine, volatiles)

Back 12

1/3

Front 13

agonists

Back 13

drugs that activate receptors

Front 14

antagonists

Back 14

drugs that bind to receptors w/out activating them, preventing agonists from stimulating them

Front 15

competitive antagonism(ex. NMBAs & Ach)

Back 15

increasing concentrations of an antagonist progressively inhibit responses to unchanging concentrations of an agonists

Front 16

noncompetitive antagonism

Back 16

high concentrations of an agonist cannot completely overcome antagonism

Front 17

additive effect
(Example: 2 inhaled anesthetics)

Back 17

two drugs produce an effect equal to algebraic summation

Front 18

synergistic effect
(Example: aminoglycoside & NMBAs)

Back 18

two drugs produce an effect more than equal to algebraic summation

Front 19

hyperreactive individuals

Back 19

usual doses of drugs prodced increased effects

Front 20

hyporeactive individuals

Back 20

usual doses of drugs produce decreased effects

Front 21

tolerance

Back 21

hyporeactivity from chronic exposure to a drug

Front 22

cross-tolerance
(ex. Inhaled anesthetics & chronic alcohol ingestion).

Back 22

develops b/t drugs of different classes that produce similar pharmacolgic effects

Front 23

tachyphylaxis
(ex. ephedrine)

Back 23

tolerance that develops acutely with only a few doses of a drug

Front 24

idiosyncrasy

what do they typically reflect?

Back 24

unusual effect of a drug in uniquely susceptible pts regardless of the dose

mostly due to hypersensitivity (allergy)or genetic differences

Front 25

dose-response curve

Back 25

shows relationship b/t dose/plasma concentration of the drug and the resulting pharmacologic effects

Front 26

what are the components of the dose response curve?

Back 26

potency
slope
efficacy
individual responses

Front 27

effective dose (ED)

Back 27

doses required to produce a specific effect

Front 28

ED50

ED90

Back 28

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

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

etc.

Front 29

what shifts the dose-response curve to the left?

Back 29

increased affinity of a drug for its receptors

Front 30

when calculating drugs by body wt, when will total body weight overestimate lean body mass?

Back 30

when body wt > ideal body wt

Front 31

at what adult wt for female and male is it rarely necessary to scale dose to body weight?

Back 31

females > 80 kg
males > 100 kg

Front 32

what influences the slope on the dose-response curve?

Back 32

the number of receptors that must be occupied before a drug effect occurs

Front 33

what dose a steep dose-response curve represent?
(ex. NMBA, inhaled agents)

Back 33

a drug must occupy a majority of the receptors before effect occurs

Front 34

when the dose-response curve is steep, small increases in doses will have what impact?

Back 34

large increases in drug effect

Front 35

what happents to the drug effect when you increase the MAC of a volatile from 1 to 1.3?

Back 35

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!

Front 36

what is negative about drugs with steep dose-response curves? what does this mean in terms of volatile agents?

Back 36

difference b/t therapeutic & toxic concentraions may be small

small difference b/t doses that produce desirable degrees of CNS depression & undesirable cardiopulmonary depression

Front 37

efficacy

Back 37

maximal effect of a drug

Front 38

on what part of the dose-reponse curve is efficacy represented?

Back 38

plateau

Front 39

what can limit dosages of drugs below concentrations associated w/ its maximal effect?

Back 39

undesirable side effects

Front 40

are efficacy and potency of drugs always related?

Back 40

no

Front 41

what 2 pharmacological principles impact individual responses to drugs. Give examples of each.

Back 41

1.pharmacokinetics
a.renal fxn
b.liver fxn
c.cardac fxn
d.age

and/or

2.pharmacodynamics
a.enzyme activity
b.genetic differences

Front 42

pharmacokinetics of IV drugs is influenced by what 2 factors?

Back 42

1. volume of distribution (Vd)
2.clearance

Front 43

elimination half-time

Back 43

rate at which plasma concentration of a durg decreases with time

Front 44

what 2 factors determine elimination half-time?

Back 44

1.volume of distribution (Vd)
2. clearance

Front 45

what 2 things are more useful than elimination half-time in characterizing clinical responses to drugs?

Back 45

1.context-sensitivity half-time
2.effect-site equilibrium time

Front 46

volume of distribution (Vd)

Back 46

dose of drug admin IV divided by plasma concentration

Front 47

what does volume of distribution reflect?

Back 47

the apparent volumes of the bodies compartments (of the compartment model) for that drug

Front 48

what 3 drug properties limit passage of drugs into tissues resulting in a small Vd?

Back 48

1.binding to plasma protein
2.high degree of ionization
3.low lipid solubility

Front 49

are the tissues peripheral or central compartments?

Back 49

peripheral

Front 50

do NMBAs have small or large Vd? why?

Back 50

small Vd

b/c they are more ionized and stay in the ECF

Front 51

is the body's circulation considered a peripheral or central compartment?

Back 51

central

Front 52

are the plasma concentrations of nonionized lipid solubles drugs high or low? why?

Back 52

low

b/c they easily pass into tissue from the circulation

Front 53

are nonionized drugs lipid or water soluble?
(ex. thiopental, diazepam)

Back 53

lipid soluble

Front 54

do nonionized drugs have large or small Vds? why?

Back 54

large

b/c they are lipid soluble

Front 55

Are volume of distributions representations of absolute anatomic volumes?

Back 55

No

Front 56

Clearance

Back 56

Volume of plasma (central compartment) cleared of drug by renal excretion and/or metabolism in liver or other organs

Front 57

What are the units for clearance?

Back 57

ml/min

Front 58

What is one of the most important pharmacokinetic variables to consider when defining a constant rate of IV drug infusion?

Back 58

Clearance

Front 59

When the rate of a drug infusion > clearance what 2 things happen?

Back 59

1.plasma concentration increase more
2.cumulative drug effects occur

Front 60

Which organ is the most important organ for clearance of unchanged drugs or their metabolites?

Back 60

Kidneys

Front 61

Which compounds are excreted more efficiently? Water soluble compounds not bound to proteins or lipid soluble protein-bound drugs

Back 61

Water soluble compounds not bound to proteins

Front 62

What 2 clinical lab indicators are useful for assessing the ability of kidneys for eliminate drugs?

Back 62

1.creatinine clearance
2.serum creatinine concentrations

Front 63

What benefit do creatinine clearance and serum creatinine concentrations have for drugs dosing?

Back 63

Provides an estimate for downward adjustments of drug dosages to prevent accumulation of drug in plasma

Front 64

What is the primary organ for metabolism?

Back 64

Liver

Front 65

What are 3 secondary organs for metabolism?

Back 65

1.kidneys
2.lungs
3.GI tract

Front 66

For water soluble drugs, are the following increased or decreased?
A.Vd
B.renal excretion

Back 66

A.Vd = decreased
B.renal excretion = increased

Front 67

For lipid soluble drugs, are the following increased or decreased?
A.Vd
B.renal excretion

Back 67

A.Vd = increased
B.renal excretion = decreased

Front 68

Why is renal excretion of lipid soluble compounds decreased? Hint: thing about kidney sites & mechanisms

Back 68

Excretion is decreased b/c of ease of reabsorption from lumens of renal tubules into pericapillary fluid

Front 69

What enzymes participate in metabolism of many drugs? And where are they located?

Back 69

Microsomal enzymes

liver

Front 70

What specific site of the liver are microsomal enzymes?

Back 70

Hepatic smooth endoplasmic reticulum

Front 71

What were microsomal enzymes derived from?

Back 71

centrifuged homogenized hepatocytes from disrupted smooth endoplasmic reticulum know as microsomal fraction containing the cytochrome P450 system

Front 72

What is the plasma concentration curve?

Back 72

A graphic plot of the logarithm of the plasma concentration of drug vs time following rapid IV (bolus) injection

Front 73

How many phases does the plasma concentration curve have? And what are they?

Back 73

2

1.Distribution (alpha) phase & 2.elimination (beta) phase

Front 74

What do the two plasma concentration curve phases characterize?

Back 74

Distribution half-time of the drug

Front 75

What does first phase distribution (alpha) phase correspond with?

Back 75

The initial distribution of drug from circulation to tissues

Front 76

What does second phase elimination (beta) phase correspond with?

Back 76

Gradual elimination in plasma concentration of drug from central vascular compartment by renal and hepatic mechanisms

Front 77

Elimination half-time

Back 77

Time needed for plasma concentration of drug to decreased 50% during elimination phase

Front 78

How many elimination half-times are needed for almost complete elimination of a drug?

Back 78

5

Front 79

What does dose intervals more frequent than 5 elimination half-times result in? (2)

Back 79

1.Accumulation of the drug
2.Cumulative drug effects

Front 80

How many elimination half-times does it take for a drug to achieve steady state plasma concentration (Cps) with intermittent doses?

Back 80

5 elimination half-times

Front 81

Which compartment model is elimination half-time more useful?

Back 81

One-compartment model (central compartment)

Front 82

Elimination half-time shows virtually no insight into rate of decrease in plasma concentration after dc of ___________.

Back 82

IV drug administration

Front 83

Context-sensitive half-time

Back 83

Time needed for drug concentration to decrease a predetermined percentage after dc of continuous IV infusion of a specific duration

Front 84

Context of context-sensitive half-time refers to?

Back 84

Duration of infusion

Front 85

What 3 things does context-sensitive half-time largely depend on?

Back 85

1.drug lipid solubility
2.efficiency of drug clearance mechanisms
3.duration of continuous IV admin

Front 86

What happens to context-sensitive half-time when duration of continuous IV administration increases?

Back 86

Increases

Front 87

is context-sensitive half-time related to elimination half-time of a drug?

Back 87

No

Front 88

In relation to drugs, what does time to recovery depend on?

Back 88

How far plasma concentration must decrease to reach levels compatible with awakening

Front 89

If concentration of drug admin by continuous infusion is just above that needed to awaken, is time to recover slow or rapid?

Back 89

Rapid

Front 90

If concentration of drug admin by continuous infusion is much higher than that needed to awaken, is time to recover slow or rapid?

Back 90

Slow

Front 91

What does BIS stand for?

Back 91

Bispectral Index

Front 92

Why is the BIS beneficial in regard to IV drugs?

Back 92

Allows more precise titration for more desired level of drug effect

Front 93

Effect-Site Equilibration time

Back 93

is time for equilibration between drug concentration in plasma and drug effect

Front 94

What’s a clinical benefit of effect-site equilibration times?

Back 94

Logical timing of IV drug admin (dosing intervals)

Front 95

Drugs with short effect-site equilibration times will produce slow or rapid onset of pharmacologic effects?
(ex. remifentanil, alfentanil, thiopental, propofol)

Back 95

Rapid

Front 96

Drugs with longer effect-site equilibration times will produce slow or rapid onset of pharmacologic effects?
(ex. fentanl, sufentanil, midazolam)

Back 96

Slow

Front 97

Nonionized

Back 97

– active and lipid soluble

Front 98

Ionized

Back 98

– inactive, and water soluble

Front 99

Degree of ionization of drug is a function of what 2 things.

Back 99

1.pK
2.pH of surrounding fluid

Front 100

What does it mean when pK and pH are identical?

Back 100

50% of drug exists in ionized form

Front 101

if pH and pK values are similar small changes in pH can result in?

Back 101

large changes in degree of ionization

Front 102

What type of drugs are highly ionized at an alkaline pH ?
(ex. barbiturates)

Back 102

Acidic drugs

Front 103

What are highly ionized at an acid pH?
(ex. opioids, local anesthetics)

Back 103

Basic drugs

Front 104

Which route of administration of drugs ensures the best achievement of predictable plasma concentration?

Back 104

IV

Front 105

Is IM admin predictable or unpredictable? And what is it dependent on?

Back 105

unpredictable

local blood flow

Front 106

What is first-pass hepatic effect?

Back 106

Drugs enter portal venous blood, passes through liver before entering systemic circulation

Front 107

What is reason for large differences between effective oral and IV doses?

Back 107

First-pass hepatic effect

Front 108

What phenomenon effects GI (small intestine) admin?

Back 108

First-pass hepatic effect

Front 109

first-pass pulmonary effect

Back 109

uptake of basic lipophilic amines (lidocaine, propranolol, fentanyl) into the lungs which serve as a reservoir to release drugs back into systemic circulation

Front 110

Following systemic absorption, which tissues receive larger amount of total dose?

Back 110

highly perfused tissues (brain, heart, kidneys, liver)

Front 111

____% of CO is delivered to about _____% of total body mass.

Back 111

75%; 10%

Front 112

redistribution

Back 112

As plasma concentration decreases below highly perfused tissues, drugs go to less perfused tissues (skeletal muscle)

Front 113

What is principally responsible for awakening after single dose of a drug?

Back 113

Redistribution

Front 114

At the cellular level how do drugs exert pharmacologic effects?

Back 114

by interacting with receptors

Front 115

Receptors

Back 115

Transmembrane protein molecules in the lipid
bilayer of the cell

Front 116

Regarding the drug-receptor interaction, what initiates or prevents a series of changes that characterize the pharmacologic effects of the drug?

Back 116

altered function or conformation of a specific cellular component

Front 117

Name 3 excitable transmembrane protein receptors.

Back 117

1.voltage-sensitive ion channels
2. Ligand-gated ion channels
3. Transmembrane receptors

Front 118

Voltage-sensitive ion channels

Back 118

ion channels that open and close depending on cell membrane voltage

Front 119

What are some examples of voltage-sensitive ion channels?

Back 119

Na, Cl, K, Ca

Front 120

Ligand-gated ion channels

Back 120

nicotinic cholinergic receptors & amino acid receptors (GABA) function as receptor-ion channel complexes

Front 121

What does GABA stand for?

Back 121

Gama-Aminobutyric Acid Receptor

Front 122

Activation of GABA results in? (3)

Back 122

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

Front 123

Give 3 examples of drugs that activate GABA

Back 123

1.benzodiazepines
2.barbiturates
3.propofol

Front 124

How many of the synapses in CNS are GABA receptors?

Back 124

Approximately 1/3 of all synapses

Front 125

Regarding the GABA receptor, what do Opioids and alpha-2 agonists do at the presynaptic site?

Back 125

may inhibit the presynaptic calcium ion channels responsible for activating neurotransmitter release

Front 126

What are G Proteins?

Back 126

important intermediaries in cell communication; second messengers

Front 127

What does G protein stand for?

Back 127

Guanine Nucleotide Proteins

Front 128

How does the mechanism of second messenger with G proteins work?

Back 128

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.

Front 129

Clinically important G Protein-coupled receptor systems? (6)

Back 129

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)

Front 130

Name the chemical name for the 2 racemic mixture components.

Back 130

the dextro (d) or levo (l) isomer

Front 131

Are the number of receptors in the body static or dynamic?

Back 131

Dynamic

Front 132

Up-Regulation

Back 132

increasing number of receptors in response to decreased stimulation

Front 133

Down-Regulation

Back 133

Decreasing number of receptors in response to increased stimulation

Front 134

steady state conditions

Back 134

plasma concentrations of drugs are proportional, or equal, to receptor concentration of drugs

Front 135

concentration of drugs at receptors will be influence by what factors? (pharmacokinetics or pharmocodynamics)

Back 135

Pharmacokinetic factors that influence plasma concentrations of drugs tissue uptake, renal excretion, hepatic metabolism)

Front 136

Relationship between plasma concentration of drugs and pharmacologic response elicited is influenced by? (pharmacokinetics or pharmocodynamics)

Back 136

Pharmacodynamics

Front 137

Pharmacokinetics of inhaled anesthetics describes?

Back 137

1.Uptake (absorption) from alveoli into systemic circulation
2.Distribution in the body
3.Elimination via lungs or metabolism (principally in liver)

Front 138

Controlling the inspired partial pressure (PI) creates what?

Back 138

a gradient so that the anesthetic is delivered from the anesthesia machine to the site of action

Front 139

The primary objective of inhalation anesthesia?

Back 139

achieve a constant & optimal brain partial pressure (Pbr) of the anesthetic

Front 140

What is PI?

Back 140

Inspired partial pressure

Front 141

What’s Pbr?

Back 141

Brain partial pressure

Front 142

What’s Pa?

Back 142

Arterial partial pressure

Front 143

What’s PA?

Back 143

Alveolar partial pressure

Front 144

What mirrors Pbr of an inhaled anesthetic?

Back 144

PA

Front 145

What 3 things is PA able to determine?

Back 145

1.index of anesthetic depth
2.rate of induction & recovery of anesthesia
3.measure of equal potency

Front 146

What Factors Determine the Alveolar Partial Pressure?

Back 146

input (delivery) into the alveoli minus uptake (loss) from alveoli into pulmonary arterial

Front 147

Input of inhaled anesthetic is dependent on what 3 things?

Back 147

1.Partial pressure inspired (PI)
2.Alveolar ventilation (VA)
3.Characteristics of anesthetic breathing system

Front 148

Uptake of inhaled anesthetic is dependent on what 3 things?

Back 148

1.Solubility
2.CO
3.Alveolar-to-venous partial pressure difference (A-vD)

Front 149

Are metabolism & percutaneous loss of inhaled anesthetics a significant influence on PA during induction & maintenance of anesthesia?

Back 149

No

Front 150

What 3 factors determine partial pressure gradients necessary for establishment of anesthesia?

Back 150

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

Front 151

What 3 things influences transfer of inhaled anesthetic from anesthetic machine to alveoli?

Back 151

a.Inspired partial pressure
b.Alveolar ventilation c.Characteristics of anesthetic breathing system

Front 152

What 3 things influence transfer of inhaled anesthetic from alveoli to arterial blood ?

Back 152

a.Blood:gas partition coefficient
b.CO
c.Alveolar-to-venous partial pressure difference

Front 153

What 3 things influence transfer of inhaled anesthetic from arterial blood to brain ?

Back 153

a.Brain:blood partition coefficient
b.Cerebral blood flow
c.Arterial-to-venous partial pressure difference

Front 154

Concentration effect
-What is it?
-What does it inevitably do?

Back 154

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.

Front 155

Why is decreasing PI after optimal PA level reached critical?

Back 155

to match decreasing uptake & maintaining a constant and optimal Pbr

Front 156

When will you decrease PI?

Back 156

as uptake into blood decreases

Front 157

Does the concentration effect and the second gas effect work dependently or independently?

Back 157

Independently

Front 158

second gas effect

Back 158

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)

Front 159

alveolar hyperoxygenation

Back 159

transient increase (about 10%) in Pao2 that accompanies early phase of nitrous oxide administration reflects second gas effect of nitrous oxide on oxygen

Front 160

Increased VA, like PI, will do what to the inhaled anesthetic, PA, and induction time? And what will have the opposite effect?

Back 160

promote input of inhaled anesthetics to offset uptake into the blood; more rapid rate of increase in PA and induction of anesthesia

hypoventilation

Front 161

How does controlled ventilation of lungs accelerates rate of increase of the PA?

Back 161

hyperventilation (increased VA) and decreased venous return(decreased CO)

Front 162

Risk of anesthetic overdose may be increased during what type of ventilation?

Back 162

controlled ventilation of lungs

Front 163

What characteristics of the anesthetic breathing system influences rate of increased of PA?

Back 163

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

Front 164

How is solubility of inhaled anesthetics in blood and tissues expressed?

Back 164

partition coefficients

Front 165

partition coefficients

Back 165

distribution ratio describing how the inhaled anesthetic distributes itself between two phases at equilibrium (when partial pressures are identical)

Front 166

What does it mean when Blood:gas partition coefficient is 10?

Back 166

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

Front 167

Partition coefficients are _________-dependent.

Back 167

temperature

Front 168

The solubility of a gas in a liquid is increased when the temperature of the liquid ___________.

Back 168

decreased

Front 169

partition coefficients are usually for what temperature, unless otherwised stated?

Back 169

37ºC

Front 170

What factor determines amount of inhaled anesthetic that must be dissolved (undergo uptake) in blood before equilibrium with gas phase is reached?

Back 170

Solubility

Front 171

Blood is considered a pharmacologically active or inactive reservoir?

Back 171

pharmacologically inactive reservoir

Front 172

the size of the resevoir provided by blood is determined by?

Back 172

the solubility of the anesthetic in the blood

Front 173

When blood:gas partition coefficient is ___ (high or low) a large amount of anesthetic must be dissolved in blood before the Pa = PA.

Back 173

high

Front 174

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.

Back 174

low

Front 175

Blood:Gas Partition Coefficients

Back 175

time necessary for equilibration of PA with Pa

Front 176

Tissue:Blood Partition Coefficients

Back 176

time necessary for equilibration of Pa with tissue

Front 177

What has to be calculated to predict tissue:blood partition coefficients?

Back 177

time constant for each tissue

Front 178

time constant

Back 178

amount of inhaled anesthetic that can be dissolved in tissue divided by tissue blood flow

Front 179

Complete equilibration of any tissue, including the brain, with the Pa requires at least how many time constants?

Back 179

three time constants

Front 180

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)?

Back 180

about 3-4 minutes

about 10-15 minutes

Front 181

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)?

Back 181

about 2 minutes

about 6 minutes

Front 182

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

Back 182

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.

Front 183

Entrance of nitrous oxide into an air-filled cavity surrounded by a ______ causes the gas space to expand. Give examples.

Back 183

compliant wall (intestinal gas, pneumothorax, pulmonary blebs, air embolism)

Front 184

Entrance of nitrous oxide into air-filled cavity by a _____ causes an increase in pressure. Give examples.

Back 184

non compliant wall(middle ear, cerebral ventricles, supratentorial subdural space)

Front 185

Magnitude of volume or pressure increase in air-fill cavity when administering nitrous oxide is influenced by what 3 things?

Back 185

1.PA of nitrous oxide

2.Blood flow to air-filled cavity

3.Duration of nitrous oxide administration

Front 186

Contraindications for nitrous oxide administration.

Back 186

1.closed pneumothorax

2.trauma (rib fractures)

3.venous air embolism

Front 187

How does high cardiac output influence rate of increase of PA and rate of anesthesia induction?

Back 187

decreased rate of increased of PA & slow induction of anesthesia

Front 188

How does slow cardiac output influence rate of increase of PA and rate of anesthesia induction?

Back 188

increased rate of increased of PA & fast induction of anesthesia

Front 189

What effect does a right-to-left intracardiac or intrapulmonary shunt have on rate of induction of anesthesia? Why?

Back 189

slows rate of induction of anesthesia

dilutional effect

Front 190

what effect does wasted ventilation (dead space) have on rate of induction of anesthesia? why?

Back 190

no effect

no dilutional effect on Pa produced

Front 191

what does Alveolar-to-Venous Partial Pressure Differences (A-vD)reflect?

Back 191

tissue uptake of inhaled anesthetics

Front 192

Skeletal muscle and fat represent about ___% of body mass, and receive less than ___% of CO.

Back 192

70%; 25%

Front 193

What tissues continue to act as inactive reservoirs for anesthetic uptake for several hours?

Back 193

Tissues like skeletal muscle and fat

Front 194

Is Equilibration of inhaled anesthetics between fat & arterial blood ever achieved?

Back 194

probably never achieved

Front 195

How can recovery from inhaled anesthesia be defined?

Back 195

rate at which the PA decreases with time

Front 196

how does recovery from anesthesia differs from induction of anesthesia ? (3)

Back 196

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

Front 197

Impact of tissue storage on recovery depends on? (2)

Back 197

a.Duration of anesthesia

b. Solubility of anesthetic in various tissue compartments

Front 198

Which agents have longest recovery more soluble or less soluble ones? Give examples.

Back 198

more soluble

more solubles = halothane, isoflurane

poorly solubles = sevoflurane and desflurane

Front 199

which volatile agent(s) is/are dependent on metabolism and VA for decrease in PA? why?

Back 199

halothane

it's a highly lipid soluble methoxyflurane

Front 200

which volatile agent(s) is/are dependent on VA for decrease in PA? why?

Back 200

isoflurane, desflurane, and sevoflurane

less lipid soluble

Front 201

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

Back 201

less than 5 minutes

no

Front 202

when does the principle difference in rates at which desflurane, sevoflurane, and isoflurane are eliminated occur?

Back 202

in the final 20% of the elimination process

Front 203

a.When does diffusion hypoxia occur? b.How does diffusion hypoxia occur?

Back 203

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.

Front 204

how can diffusion hypoxia be prevented?

Back 204

by filling patients lungs with oxygen at conclusion of nitrous oxide administration.

Front 205

What does MAC stand for?

Back 205

Minimum Alveolar Concentration

Front 206

MAC

Back 206

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.

Front 207

WHy is MAC the most useful index of anesthetic equal potency for comparison between inhaled anesthetics?

Back 207

because MAC reflects the partial pressure at the anesthetic site of action (Pbr)

Front 208

Are MAC values for combinations of inhaled anesthetics synergistic or additive?

Back 208

additive

Front 209

the MAC for volatile anesthetics is decreased about ___% for every ___% alveolar nitrous oxide concentration used.

Back 209

1;1

Front 210

give the reason for administering nitrous oxide with volatile anesthetics.

Back 210

depression of ventilation and circulation is less when nitrous oxide is substituted for an equivalent MAC dose of volatile drug.

Front 211

how much MAC required to prevent skeletal muscle movement in response to painful stimulation in nearly all patients during surgery?

Back 211

1.3 MAC

Front 212

Name some Physiologic and Pharmacologic Factors that have no impact on MAC. (8)

Back 212

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

Front 213

Name some Physiologic and Pharmacologic Factors that increase MAC. (5)

Back 213

1.Hyperthermia
2.Drugs that increase CNS catecholamines (MAOI’s, Tricyclic antidepressants, Cocaine, Acute amphetamine ingestion)
3.Infants
4.Hypernatremia
5.Chronic ethanol abuse

Front 214

Name some Physiologic and Pharmacologic Factors that decrease MAC. (14)

Back 214

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

Front 215

Lack of Skeletal muscle responses with inhaled anesthetic may be mediated where?

Back 215

spinal cord

Front 216

Amnesia responses of inhaled anesthetics may result from actions at?

Back 216

supraspinal sites in a nonpolar environment

Front 217

anesthetic drug-induced inhibition of synaptic transmission through what?

Back 217

multineuronal polysynaptic pathways, especially the reticular activating system

Front 218

what's the other name for Myer-Overton Theory?

Back 218

(Critical-Volume Hypothesis)

Front 219

What are the 2 principles of Myer-Overton Theory?

Back 219

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.

Front 220

Isoflurance
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?

Back 220

a. 1.46
b. 1.17
c. yes

Front 221

Enflurane
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?

Back 221

a. 1.9
b. 1.63
c. yes

Front 222

Halothane
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?

Back 222

a. 2.54
b. 0.75
c. no (Halothane hepatitis)

Front 223

Desflurane
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?

Back 223

a. 0.42
b. 6.6
c. yes

Front 224

Sevoflurane
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?

Back 224

a. 0.69
b. 1.8
c. no (Compound A, nephrotoxic)

Front 225

Nitrous oxide (NO2)
a.blood:gas partition coeff
b.MAC
c.stable in soda lime?

Back 225

a. 0.46
b. 104
c. yes