Inhaled Anesthetics

Question 1

Where is the most important site of action of volatile anesthetics associated with immobilization?

Answer 1

Spinal cord

Question 2

Volatile inhaled anesthetics enhance inhibitory synaptic transmission postsynaptically by …, extrasynaptically by …, and presynaptically by …

Answer 2

• potentiating ligand-gated ion channels activated by γ-aminobutyric acid (GABA) and glycine
• enhancing GABA receptors
• enhancing basal GABA release

Question 3

Actions at GABAA receptors appear to be important for the end point of immobility of inhalational agents

T or F

Answer 3

F

actions at GABAA receptors appear not to be important for the end point of immobility, at least where inhalational agents are concerned

Question 4

Actions at GABAA receptors appear to be important for the end point of immobility of inhalational agents

T or F

Answer 4

F

actions at GABAA receptors appear not to be important for the end point of immobility, at least where inhalational agents are concerned

Question 5

Which molecular structures may be associated with the immobility caused by de volatile anesthetics?

Answer 5

voltage-gated sodium (Na+) channels

tandem-pore domain potassium channels (K2P)

Question 6

Molecular structures associated with the anterograde amnesia caused by de volatile anesthetics

Answer 6

Enhancement of GABAergic inhibition can account for a substantial portion of isoflurane’s effect on memory.

Other contributing targets may include nAChRs, HCN1 (Potassium/sodium hyperpolarization-activated cyclic nucleotide-gated channel 1) channels, and excitatory glutamatergic synapses

Question 7

Recovery from sleep deprivation can occur under propofol but does not occur with inhalational anesthesia

T or F

Answer 7

F

recovery from sleep deprivation can occur under propofol and inhalational anesthesia

Question 8

A convergence of x-ray crystallography, molecular modeling, and structure-function studies indicates that inhaled anesthetics bind in the … proteins.
The lipophilic (or hydrophobic) nature of these binding sites explains their adherence to the … correlation

Answer 8

hydrophobic cavities formed within

Meyer-Overton

Question 9

GABAA receptors are the principal transmitter-gated Cl− channels in the…, whereas GlyRs (glycine receptors) fulfill this function in the …, with some overlap in the …

Answer 9

neocortex and allocortex

spinal cord

diencephalon and brain stem

Question 10

Most functional GABAA and GlyRs are heteropentamers, typically consisting of three different GABAA subunits (e.g., …) or two different GlyR subunits (…)

Presence of a … subunit is required for benzodiazepine modulation of GABAA receptors and can also influence modulation by inhaled anesthetics

Answer 10

two α, two β, and one γ or ∂

three α and two β

γ

Question 11

The related cation-permeable 5-hydroxytryptamine (serotonin)-3 (5HT3) receptors are potentiated by volatile anesthetics. 5HT3 receptors are involved with … and also probably contribute to the … of volatile anesthetics

Answer 11

Autonomic reflexes

emetogenic properties

Question 12

NMDA receptors are a major postsynaptic receptor subtype of inotropic receptors for glutamate, the principal excitatory neurotransmitter in the mammalian CNS.
Typical NMDA receptors, defined pharmacologically by their selective activation by the exogenous agonist NMDA, are heteromers consisting of an obligatory … subunit and modulatory … subunits.
Channel opening requires glutamate (or another synthetic agonist such as NMDA) binding to the … subunit while the endogenous coagonist glycine binds to the … subunit. NMDA receptors also require membrane depolarization to relieve voltage-dependent block by …. Depolarization is typically provided by the binding of glutamate to non-NMDA glutamate receptors

Answer 12

GluN1

GluN2

GluN2

GluN1

Mg2+

Question 13

Inhaled anesthetics suppress excitatory synaptic transmission presynaptically by … (volatile anesthetics) and postsynaptically by … (gaseous and to some extent volatile anesthetics).

Answer 13

reducing glutamate release

inhibiting excitatory ionotropic receptors activated by glutamate

Question 14

Distinct voltage-gated Ca2+ channel subtypes are expressed in various cells and tissues, and are classified pharmacologically and functionally by the degree of depolarization required to gate the channel as low voltage–activated (LVA; … ) or high voltage–activated (HVA; … ) channels

Answer 14

T-type

L-, N-, R-, and P/Q-type

Question 15

At higher doses, a role for Ca2+ channel inhibition in the negative inotropic effects of volatile anesthetics is well established.
The force of myocardial contraction is determined by the magnitude of cytosolic Ca2+ increase after electrical excitation, the responsiveness of the contractile proteins to Ca2+, and sarcomere length. Negative inotropic effects of volatile anesthetics are mediated by … .
Volatile anesthetics reduce the Ca2+ transient and shorten action potential duration in cardiomyocytes primarily by inhibiting … currents, resulting in a negative inotropic effect and arrhythmogenicity

Answer 15

reductions in Ca2+ availability, Ca2+ sensitivity of the contractile proteins, and rate of cytosolic Ca2+ clearance

L-type (Cav1.2) Ca2+

Question 16

Malignant hyperthermia is a pharmacogenetic disorder that manifests as a potentially fatal hypermetabolic crisis triggered by volatile anesthetics, particularly halothane. It is often associated with mutations in … and the physically associated … channel (Cav1.1), which functions as the voltage sensor. Volatile anesthetics activate the mutated …, resulting in uncontrolled intracellular Ca2+ release from the SR, muscle contraction, and hypermetabolic activity

Answer 16

RyR1

L-type Ca2+

RyRs

Question 17

How do volatile anesthetics can cause intracellular calcium stores depletion?

Answer 17

Intracellular Ca2+ channels regulate Ca2+ release from intracellular stores, particularly the ER and sarcoplasmic reticulum (SR). These include 1,4,5-inositol triphosphate receptors (IP3Rs), regulated by the second messenger IP3, and ryanodine receptors (RyRs); the latter mediate the release of SR Ca2+, which is critical to excitation-contraction coupling in muscle. Volatile anesthetic–induced Ca2+ leak occurs by effects on both IP3R and RyR channels, which leads to depletion of intracellular Ca2+ stores from the SR and ER

Question 18

Activation of K2P channels by volatile and gaseous anesthetics―including xenon, nitrous oxide, and cyclopropane―was observed in mammals. Increased K+ conductance can …, reducing responsiveness to excitatory synaptic input and possibly altering network synchrony. Targeted deletion of the TASK-1, TASK-3, and TREK-1 K2P channels in mice reduces sensitivity to … by volatile anesthetics in an agent-specific manner, implicating these channels as contributory anesthetic targets in vivo.
The K+ channel TREK-1 also contributes to the … effects of xenon and sevoflurane

Answer 18

hyperpolarize neurons

immobilization

neuroprotective

Question 19

Volatile anesthetics and xenon activate cardiac mitochondrial and sarcolemmal KATP channels,which might contribute to …

Answer 19

anesthetic preconditioning to cardiac ischemia

Question 20

Volatile anesthetics have a relatively … potency but … efficacy at synaptic GABAA receptors and a … potency and … efficacy at extrasynaptic GABAA receptors

Answer 20

low

high

high

low

Question 21

Excitatory synaptic excitation is generally decreased by volatile anesthetics. Experiments in various slice preparations indicate that reduced excitation is primarily caused by … mechanisms.

By contrast, the effects of the nonhalogenated inhaled anesthetics (xenon, nitrous oxide, cyclopropane)
appear to be mediated primarily by inhibition of …

Answer 21

presynaptic

postsynaptic NMDA receptors

Question 22

Oscillations with EEG frequencies from 1.5 to 4 Hz are generally referred to as …, and these oscillations are characteristic of … and are commonly observed under general anesthesia. Even slower rhythms (below 1 Hz) occur during … sleep and appear at loss of consciousness induced by propofol and sevoflurane

Answer 22

δ-rhythms

deep sleep

non–rapid eye movement (NREM)

Question 23

θ-Rhythms, present in various cortical structures but most prominent in the hippocampus, are thought to signal the “online state.” They are associated with … during waking behavior. One component of the θ-rhythm (type I or …) can be affected by amnestic concentrations of isoflurane as well as by the amnestic nonimmobilizer F6, indicating a potential network-level signature effect for anesthetic-induced amnesia. Type II θ-rhythm (…) can be evoked under anesthesia and is slowed and potentiated by halothane.

Answer 23

sensorimotor and mnemonic functions

atropine-resistant

atropine-sensitive

Question 24

The blood solubility of anesthetic gases (and other gases such as O2, N2, and CO2) increases as temperature …

Answer 24

decreases

Question 25

Anesthetic partitioning into blood (blood solubility) increases after ingestion of fatty foods and may decrease in anemic or malnourished patients

T or F

Answer 25

T

Question 26

During an inhaled anesthetic induction, the rate of increase of Palv relative to Pcirc is governed by …

Answer 26

(1) alveolar ventilation, (2) cardiac output, and (3) anesthetic solubility in blood.

Increased ventilation delivers more anesthetic from circuit to alveoli and increases Palv/Pcirc.

Importantly, increased pulmonary blood flow removes more anesthetic from alveoli, thereby decreasing the rate of increase in alveolar concentration of anesthetic (Palv/Pcirc). Indeed, significant decreases in cardiac output are suspected when end-tidal CO2 (ETCO2) decreases and end-tidal concentration of VA increases.

The more soluble an anesthetic is in blood (i.e., the higher its λb/g), the greater is the capacity for each volume of blood to take up anesthetic from alveolar gases (i.e., the larger the effective blood flow). Thus as λb/g increases, Palv/Pcirc increases more slowly

Question 27

How does dead space affect the volatile anesthetics uptake?

Answer 27

Dead space (ventilated but not perfused pulmonary regions) reduces effective alveolar ventilation, and thus slows anesthetic uptake

Question 28

How shunting affect the induction with volatile anesthetics?

Answer 28

Pulmonary right to left shunting can be physiologic, pathologic, or iatrogenic, such as during one-lung ventilation. Right-to-left shunting results in a difference between Palv and the partial pressure of anesthetic in arterial blood (Part). This is because arterial blood represents a mixture of shunted mixed venous blood combined with blood that has equilibrated with alveolar gases. Because such shunts also reduce transcapillary gas exchange in the lung and slow anesthetic uptake, right-to-left shunting sustains Pcirc, an effect that is more pronounced for highly soluble drugs compared with insoluble anesthetics. Thus shunt reduces the ratio of Part:Palv more for insoluble anesthetics, such as N2O

Question 29

Explain the concentration effect and the second gas effect

Answer 29

When the anesthetic represents a large fraction of the inhaled gas mixture, its rapid uptake results in a smaller relative alveolar anesthetic concentration drop, because the volume of alveolar gas also decreases. This is known as the concentration effect.

The second gas effect is a consequence of the concentration effect.

Ex.: After an initial inspiratory breath, alveoli are filled with the gas mixture in the circuit (66% N2O, 33% O2, 1% Isoflurane) at their normal end-inspiratory volume. After half of the N2O and isoflurane are absorbed into pulmonary blood, the alveolar gas volume is reduced by 33.5%. At this point, the volume of N2O equals the volume of O2 and the gas mixture is 49.6% N2O, 49.6% O2, 0.8% isoflurane. Inflow of additional inspired gas mixture returns alveolar volume to its original value, resulting in a gas mixture of 55.1% N2O, 44.1% O2, 0.8% isoflurane. The alveolar partial pressure of N2O falls much less than the fractional uptake (the concentration effect). In addition, the partial pressure of O2 increases relative to the inspired gas O2 content, and the partial pressure of isoflurane is sustained close to the inspired value, increasing its rate of uptake (the second gas effect)

Question 30

Traditionally, anesthetic distribution has been described for four distinct tissue groups. Describe them

Answer 30

1) The vessel-rich group (VRG):
the heart, brain, lungs, spinal cord, liver, and kidney. Together, these organs compose approximately 10% of the adult human body mass; however, they receive approximately 70% of cardiac output under normal resting conditions. As a result, time constants for anesthetic equili- bration between blood and these organs are typically only a few minutes

2) skeletal muscle:
Muscle composes approximately 40% of body mass in a healthy adult, making muscle the largest single compartment based on weight. Moreover, most inhaled anesthetics partition into muscle more than into brain, resulting in an increased effective volume for anesthetic uptake into this compartment. At rest, muscle receives about 10% to 15% of cardiac output (20 mL/kg/min), but this value can increase dramatically during exercise, stress, fever, or other states associated with high cardiac output. Taken together, these factors generally result in slow equilibration between anesthetic in blood and muscle, with typical time constants of hours.

3) fat:
in a healthy adult composes less than 25% of body mass and receives approximately 10% of cardiac output. Potent VAs partition avidly into fat; therefore, fat represents the largest effective volume for uptake of these drugs. The extremely large effective volume coupled with low blood flow results in very slow equilibration of anesthetics between blood and fat, with time constants approaching days

4) vessel poor tissues:
skin, cortical bone, and connective tissue

Question 31

Inhaled anesthetic induction in children is faster or slower than in adults? Explain

Answer 31

In pediatric patients, the balance of cardiac output to various tissue beds differs from that in adults. Thus, although cardiac output per kilogram body weight is larger in children than in adults, anesthetic induction in young children is more rapid than in adults, because a disproportionate amount of perfusion goes to the vessel rich organs, such as the brain.

Question 32

What is the MAC-awake? What is its value?

Answer 32

The alveolar anesthetic concentration preventing percep- tive awareness in 50% of subjects.

MAC-awake for potent VAs is typically 0.34 × MAC-immobility, whereas MAC- awake for N2O is approximately 0.7 × MAC-immobility

Question 33

The rate of N2O diffusion into gas-filled spaces in the body depends on … .

Thus small air emboli expand within seconds, because they have high … and are surrounded by a very high …

Answer 33

local blood flow and the surface to volume ratio of the space

surface/volume ratios

relative flow of blood containing dissolved N2O

Question 34

Unlike what happens during the induction with volatile anesthetic, an increased cardiac output increases clearance of volatile anesthetics.

T or F

Answer 34

F

increased cardiac output slows clearance, because more gas-exchange volumes are required to remove anesthetic from the larger blood flow

Question 35

Describe the diffusion hypoxia

Answer 35

Diffusion hypoxia is another sequelae of rapid outgassing from the tissues of patients anesthetized with N2O. During the initial 5 to 10 minutes after discontinuation of anesthesia, the flow of N2O from blood into the alveoli can be several liters per minute, resulting in dilution of alveolar oxygen. Another effect of rapid outgassing is reduction of alveolar PCO2, which may also reduce respiratory drive. If the patient does not receive supplemental oxygen during this period, then the combined effects of respiratory depression from anesthesia, reduced alveolar PCO2, and reduced alveolar PO2 can result in hypoventilation and oxyhemoglobin desaturation

Question 36

How diffusion hypoxia can be avoided?

Answer 36

This outcome is avoided by routinely providing supplemental O2 for the first 5 to 10 minutes of recovery, together with vigilant attention to respiration and oxygenation

Question 37

Extent of tissue metabolism (%) of volatile anesthetics

Answer 37

Extent of tissue metabolism (%)

Halothane 25
Methoxyflurane 70
Enflurane 2.5
isoflurane 0.2
Desflurane 0.02
Sevofluarane 5

Question 38

Oxidizing enzymes that paticipate of the metabolization of all halogenates

Answer 38

CYP2E1

Question 39

Volatile anesthetics that result in Trifuoroacetylated hepatocellular proteins

Answer 39

Halotane +++++
Enflurane ++
Isoflurane +
Desflurane +

Question 40

Regarding volatile anesthetics, the major oxidative enzyme … is inducible by … and is inhibited by …

Answer 40

CYP2E1

ethanol and isoniazid

disulfiram

Question 41

Clinical exposure to halothane is associated with two distinct types of hepatic injury. Describe then

Answer 41

1) Subclinical hepatotoxicity:
occurs in 20% of adults who receive halothane. It is characterized by mild postoperative elevations in alanine aminotransferase (ALT) and aspartate aminotransferase (AST), but is reversible and innocuous. Anaerobic halothane reduction by CYP2A6 to a 2-chloro-1,1,1-trifluoroethyl radicalis thought to mediate this mild hepatic injury.

2) Fulminant form of hepatotoxicity, commonly known as halothane hepatitis:
Is characterized by elevated ALT, AST, bilirubin, and alkaline phosphatase levels, and massive hepatic necrosis following the administration of halothane. Halothane hepatitis is rare (1 in 5000-35,000 administrations in adults) but is fatal in between 50% to 75% of cases. Because of the potential for fatal hepatitis, halothane is no longer used in adult patients in most countries.
Halothane hepatitis is caused by a hypersensitivity reaction associated with oxidative metabolism of halothane. The highly reactive trifluoroacetyl chloride metabolite of halothane oxidation can react with nearby liver proteins. In most patients who developed hepatic necrosis after halothane anesthesia, antibodies against trifluoro-acetyl-modified proteins were detected, suggesting that the hepatic damage is linked to an immune response against the modified protein, which acts as a neoantigen.

Question 42

Unlike all other VAs, sevoflurane is oxidized at the fluoromethoxy C-H bond and forms…

… is relatively stable, and modified liver proteins are not formed after sevoflurane anesthesia. Cases of hepatitis and rapid death after sevoflurane anesthesia have been reported, but there was no evidence of an immune-mediated mechanism

Answer 42

hexafluoroisopropanol and inorganic F−

Hexafluoroisopropanol

Question 43

Renal adverse effect caused by methoxyflurane

Answer 43

polyuric renal insufficiency

Question 44

Inorganic fluoride released during methoxyflurane metabolism probably causes renal injury, and the nephrotoxic threshold for plasma F− is approximately …

Answer 44

50 μM (microMol/liter)

Question 45

Compared with methoxyflurane, the absence of renal toxicity with newer volatile halogenated agents likely derives from a combination of factors:

Answer 45

(1) their lower tissue solubilities, particularly in kidney, resulting in lower intrarenal fluoride production;
(2) lower overall degrees of biotransformation;
(3) more rapid respiratory clearance from the body

Question 46

Halogenated anesthetics can undergo chemical breakdown while interacting with carbon dioxide (CO2) absorbents that contain strong bases such as …, which are present in soda lime and Baralyme.Strong bases extract a proton from the isopropyl group of sevoflurane, primarily forming …

Answer 46

sodium hydroxide (NaOH) and potassium hydroxide (KOH)
——
a haloalkene [fluoromethyl-2,2-difluoro-1-(trifluoromethyl) vinyl ether], known as compound A

Question 47

Compound A exposure is nephrotoxic in laboratory animals, causing … and, with sufficient exposure, death

Answer 47

proximal tubular necrosis

Question 48

In the presence of strong bases in dry CO2 absorbents (water content < … %), some halogenated VAs undergo degradation, resulting in the formation of …

Answer 48

5

CO, trifluoromethane (CF3H), and hydrogen fluoride (HF)

Question 49

The factors that determine the amount of CO produced include the chemical makeup of CO2 absorbent (… [decrescent order of the bases]), dryness of the absorbent material, the concentration of volatile agent, and its chemical structure

Answer 49

KOH > NaOH»Ba(OH)2, Ca(OH)2

Question 50

The anesthetics that contain a difluoromethyl group (difluoromethyl-ethyl ethers) are most susceptible to degradation with CO production. For these drugs CO production correlates with anesthetic concentration in the breathing circuit ( … > … > …).

… also degrade in the presence of strong bases, but do not produce CO

Answer 50

desflurane

enflurane

isoflurane

Sevoflurane, methoxyflurane, and halothane

Question 51

How can N2O cause hematologic and neurological disorders?

Answer 51

N2O is unique among anesthetics in irreversibly inhibiting cobalamins (vitamin B12) by oxidizing the Cobalt (I) ligand.
Cobalamins are ingested or produced by bacteria in the gut and are critical cofactors together with 5-methyltetrahy-drofolate in the activity of methionine synthase. Methionine synthase catalyzes methylation of homocysteine to methionine, while demethylating 5-methlytetra-hydrofolate to tetrahydrofolate. Methionine, converted to S-adenosylmethionine, is the major substrate for methylation in biochemical pathways involved in the synthesis of DNA, RNA, myelin, and catecholamines. Chronic vitamin B12 deficiency (as in pernicious anemia) results in hematologic and neurologic dysfunction.
Long-term N2O exposure, typically among individuals who frequently inhale it as a recreational drug, can also cause megaloblastic anemia, myelopathy (subacute combined degeneration), neuropathy, and encephalopathy, sometimes presenting as psychosis

Question 52

Risk factors that increase susceptibility to N2O toxicity include

Answer 52

pernicious anemia or other gastrointestinal malabsorption syndromes, extremes of age, alcoholism, malnutrition, a strict vegetarian diet, and inborn deficiencies in cobalamin or tetrahydrofolate metabolism.
Inhibitors of folate metabolism, such as methotrexate, may also enhance sensitivity to N2O toxicity

Question 53

A consequence of reduced methionine synthase activity is accumulation of its substrate: …

Answer 53

homocysteine

Question 54

Positives points of xenon in anesthesia

Answer 54

It is most comparable to N2O, but superior in a number of ways. Xenon is present as a minor constituent of air (50 parts per billion), and is isolated by distillation of liquefied air, along with liquefied nitrogen and oxygen. Xenon is entirely unreactive in the biosphere and is the only inhaled anesthetic that is not an environmental pollutant, although its distillation from air uses considerable energy and thus creates CO2 and other pollutants as byproducts.

It is odorless, tasteless, nonflammable, and has a limitless shelf-life. Its solubility in blood (λb/g = 0.14) and body tissues is lower than that of any other inhaled anesthetic, including N2O. As a result, it has extraordinarily rapid onset and respiratory clearance, with emergence times 2- to 3-fold faster
when it replaces N2O in clinical settings.

It undergoes no biotransformation or reactions with CO2 absorbents or ultraviolet light. Moreover, xenon has favorable pharmaco-dynamic effects in comparison to most inhaled anesthetics. It produces minimal cardiovascular depression and is not arrhythmogenic.

As with N2O, xenon has analgesic activity and reduces intraoperative opioid requirements.

It does not trigger malignant hyperthermia or produce any known toxicity. In fact, xenon has been shown to have cardioprotective and neuroprotective activities in preclinical models.

Clinical trials in adult cardiac surgery patients, partial nephrectomy patients, and comatose survivors of cardiac arrest have demonstrated that xenon reduces pressor requirements and modestly reduces the extent of organ damage, relative to other anesthetics. However, in these clinical settings and in others, xenon does not improve neurocognitive function or survival

Question 55

Negative points of xenon in anesthesia

Answer 55

It’s expensive: more than $15/L in the gas form, xenon is greater than 100-fold more expensive than N2O and far more expensive per patient than either desflurane or sevoflurane, which are currently the most expensive VAs.

Xenon has a MAC-immobility of 0.61 atm, and even with a strict closed- circuit technique, greater than 10 L are needed to anesthetize a typical patient.

To perform closed circuit anesthesia with xenon-oxygen also requires lengthy preanesthetic denitrogenation to prevent N2 from accumulating in the rebreathing circuit.
Transitioning from 100% oxygen during denitrogenation to closed circuit xenon-oxygen anesthesia is another slow process because xenon is added to the circuit as oxygen is metabolized in the patient at 200 to 250 mL/min. High-flow xenon is otherwise necessary to make this transition short

Xenon gas has a much higher density (5.9 g/L) than either N2O (1.9 g/L) or air (1.2 g/L), resulting in increased flow resistance and work of breathing. Thus it may be a poor choice for patients with compromised respiratory function.

As with N2O, high xenon partial pressures needed for anesthesia cause expansion of trapped air spaces and vascular air emboli.

Compared with propofol infusion or sevoflurane inhalation, xenon anesthesia results in a higher incidence of nausea and vomiting

Question 56

bronchospasm develops in about … % of asthmatics in the perioperative period

Answer 56

9

Question 57

Asthmatic bronchiolar constriction involves complex interactions of airway nerves, smooth muscle, epithelium, and inflammatory cells. In contrast, reflex bronchoconstriction caused by airway irritation is mediated by …

Answer 57

sensory afferents in the nucleus of the solitary tract (NTS), projecting to vagal preganglionic neurons (VPN)

Question 58

Vagal Preganglionic Neurons projections to the airways release acetylcholine (ACh) predominantly onto … receptors, inducing bronchoconstriction.

Answer 58

M3

Question 59

Volatile anesthetics produce bronco… through…

Volatile anesthetics also attenuate an increase in … induced by chemical and mechanical stimulation

Answer 59

dilation

decreases in cytoplasmic ionized calcium concentration and/or a reduction in calcium sensitivity of airway smooth muscle

pulmonary airway resistance

Question 60

Rooke and associates compared the bronchodilating effects of halothane, isoflurane, sevoflurane, desflurane, and thiopental–nitrous oxide in healthy patients undergoing induction of anesthesia and tracheal intubation. In contrast to thiopental–nitrous oxide, all volatile agents with the exception of … significantly reduced respiratory resistance

Answer 60

desflurane

Question 61

In children undergoing elective imaging studies, sevoflurane produced progressive reductions in the cross-sectional area of upper airway, resulting in …

Answer 61

pharyngeal airway collapse

Question 62

In healthy children, sevoflurane and desflurane slightly decreased airway resistance

T or F

Answer 62

F

In healthy children, sevoflurane slightly decreased airway resistance, but desflurane had the opposite effect, presumably via reduced airway size.

Children with documented airway susceptibility, such as those with asthma or a recent upper respiratory tract infection, exhibit significant increases in airway resistance. In these pediatric patients, desflurane should be avoided

Question 63

Volatile anesthetic–induced reductions in SR Ca2+ appear to occur through …

Answer 63

enhancement of IP3 and ryanodine-receptor channel activities

Question 64

Halothane, sevoflurane, and, minimally, isoflurane exert direct effects on muscarinic receptor–mediated contraction of isolated airway smooth muscle. The inhibitory effects of volatile agents on the biochemical coupling between the M3 muscarinic receptor and the Gαq heterotrimeric G protein is irreversible with time

T or F

Answer 64

F

Halothane, sevoflurane, and, minimally, isoflurane exert direct effects on muscarinic receptor–mediated contraction of isolated airway smooth muscle. The inhibitory effects of volatile agents on the biochemical coupling between the M3 muscarinic receptor and the Gαq heterotrimeric G protein is completely REVERSIBLE with time

Question 65

The bronchodilatory effect of volatile anesthetics is also mediated by GABA A (GABAA) receptors in the … or GABA B (GABAB) receptors on … similar to the observations with propofol

Answer 65

brainstem

preganglionic cholinergic nerves in the lung

Question 66

Effects of inhaled anesthetics on mucociliary function

Answer 66

Volatile anesthetics and nitrous oxide diminish the rates of mucous clearance by decreasing ciliary beat frequency, disrupting metachronism, and altering the physical characteristics or quantity of mucus

Question 67

Among the volatile anesthetics, … exhibited the weakest cilioinhibitory effects in rat cultured tracheal epithelial cells in vitro

Answer 67

sevoflurane

Question 68

Prolonged administration of volatile anesthetics may produce mucous pooling and impair alveolar cell surfactant metabolism

T or F

Answer 68

T

Question 69

An acute increase in PVR (pulmonary vascular resistance) can be caused by large tidal volumes, high positive end-expiratory pressure, alveolar hypoxia, hypercarbia, acidosis, and critical closing pressure

T or F

Answer 69

T

Question 70

Hypoxic pulmonary vasoconstriction (HPV) is unique to the pulmonary circulation because other vascular beds (e.g., coronary and cerebral) dilate in response to hypoxia

T or F

Answer 70

T

Question 71

Hypoxic pulmonary vasoconstriction is a locally mediated phenomenon that occurs when alveolar O2 tension falls below approximately … mm Hg and is maximal when O2 tension is approximately … mm Hg

Answer 71

60

30

Question 72

Inhaled anesthesias effects in the Hypoxic pulmonary vasoconstriction

Answer 72

Although inhibition of hypoxic pulmonary vasoconstriction by volatile anesthetic is an overall small effect, it can contribute to worsening of hypoxemia in patients with underlying pulmonary disease

Question 73

Volatile anesthetics suppress conscious control of breathing at concentrations of less than … MAC and completely abolish conscious breathing drive at higher concentrations.

All volatile anesthetics also cause a dose-dependent decrease in minute ventilation at concentrations greater than .. MAC because of a decrease in …

The respiratory rate typically … for all inhalational agents tested, except for …, which causes a significant … in respiratory rate

Answer 73

1

1

tidal volume

increases

xenon

reduction

Question 74

Describe the inhaled anesthetics effects on chemoreceptors

Answer 74

Volatile anesthetics impair peripheral chemoreceptor responses to hypoxia and hypercarbia in a dose dependent manner. In the presence of volatile anesthetic concentrations of 1 MAC or higher, breathing in humans is entirely dependent on the automatic control from the pontomedullary respiratory center and afferent excitatory inputs from the central chemoreceptors. These anesthetic concentrations lead to a complete depression of the peripheral chemoreflex loop with further respiratory depression rather than
stimulation in response to hypoxia. Even very low concentrations of the agent (0.1 MAC of isoflurane and sevoflurane) depress the peripheral chemoreflex loop, without affecting the central chemoreflex loop

Question 75

Volatile anesthetics, such as halothane, depress various respiratory muscles differently. The diaphragm, as the main inspiratory muscle, is unique in that regard because it is the respiratory muscle
most affected by volatile anesthetics, resulting in important depression

T or F

Answer 75

F

Volatile anesthetics, such as halothane, depress various respiratory muscles differently. The diaphragm, as the main inspiratory muscle, is unique in that regard because it is relatively spared from the respiratory depression by volatile anesthetics

Question 76

Volatile anesthetics (≥ … MAC) progressively abolish defensive airway reflexes.

Lower concentrations of volatile anesthetics may … protective defensive reflexes

Answer 76

1-1.3

paradoxically enhance and prolong the duration of

Question 77

Not all volatile anesthetics are equally prone to elicit unwanted sustained defensive airway reflexes.
… appear to be the most irritating VAs to the airways

Answer 77

Desflurane and isoflurane

Question 78

A recent meta-analysis concluded that xenon anesthesia provides more stable intraoperative blood pressure, lower heart rate, and faster emergence from anesthesia than volatile agents and propofol, but xenon is associated with a higher risk of …

Answer 78

PONV

Question 79

Xenon is a week parasympathetic stimulant, thus it maintains systolic, diastolic, and mean arterial blood pressures and reduces heart rate

T or F

Answer 79

F

Xenon is a SYMPATHETIC stimulant and better maintains systolic, diastolic, and mean arterial blood pressures and reduces heart rate

Question 80

Xenon is the only inhalational anesthetic that causes a decrease in respiratory rate

T or F

Answer 80

T