Chapter 4: Stoelting Inhaled Anesthetics Flashcards

Question

Is enflurane commonly used in the United States currently?

Answer 1

Enflurane is no longer in common use in the United States.

Answer 2

- Is a halogenated methyl ethyl ether. - existing as a clear, nonflammable liquid at room temperature - with a pungent, ethereal odor - It has intermediate solubility in blood and high potency, facilitating intermediate onset and recovery from anesthesia.

Answer 3

- Extremely stable - showing no detectable deterioration over 5 years of storage, even when exposed to carbon dioxide absorbents or sunlight. - Its stability negates the need for preservatives like thymol in its commercial form.

Answer 4

- Desflurane, a fluorinated methyl ethyl ether - Has a fluorine atom instead of a chlorine atom on its alpha-ethyl component. - This fluorination increases vapor pressure - Enhances molecular stability - Decreases potency

Answer 5

- Its high vapor pressure is three times that of isoflurane - Would cause it to boil at normal operating room temperatures. - Special heated and pressurized vaporizers that require electrical power are used to regulate its concentration.

Answer 6

- Desflurane is minimally metabolized, with serum and urinary concentrations of trifluoroacetate - Significantly lower than those from isoflurane metabolism. - Its potency, as indicated by MAC, is about fivefold less than isoflurane.

Answer 7

- Desflurane's pungency makes inhalation induction unpleasant - Cause airway irritation - Increasing the risk of salivation, breath holding, coughing, or laryngospasm - It also produces the highest carbon monoxide concentrations when degraded by strong bases in desiccated carbon dioxide absorbents.

Answer 8

- Pulse oximetry can't differentiate between carboxyhemoglobin and oxyhemoglobin, - Making it difficult to detect carbon monoxide exposure intraoperatively. - **Low pulse oximetry** readings despite adequate arterial oxygen **may suggest carbon monoxide exposure**.

Answer 9

- **Decreased pulse oximeter readings** - **Erroneous gas analyzer readings** (indicating mixed gases or enflurane when desflurane is used) - Can be early warnings of carbon monoxide formation attributed to trifluoromethane production.

Answer 10

- Carboxyhemoglobin can be measured acutely **with CO-oximetry** - A technology that is routinely available, to confirm carbon monoxide exposure

Answer 11

Delayed neurophysiologic sequelae such as: * Cognitive defects * Personality changes * Gait disturbances * May occur 3 to 21 days after anesthesia due to carbon monoxide poisoning.

Answer 12

- Desflurane has a **blood:gas** partition coefficient of **0.42** - **MAC of 6.6%**, allowing for rapid achievement of the necessary alveolar partial pressure for anesthesia - Prompt awakening upon discontinuation.

Answer 13

- Sevoflurane, a fluorinated methyl isopropyl ether - Has vapor pressure similar to halothane and isoflurane - Allowing use with conventional vaporizers. - Its solubility ensures quick induction and recovery. - It is nonpungent, minimally odorous, and causes less airway irritation.

Answer 14

- Recovery from sevoflurane is 3 to 4 minutes faster than isoflurane - Especially noticeable in **surgeries longer than 3 hours**

Answer 15

- Sevoflurane undergoes more metabolism than desflurane (3% to 5% biodegradation), - Produce inorganic fluoride and hexafluoroisopropanol. - It doesn't form reactive acyl halide intermediates or stimulate antitrifluoroacetylated protein antibodies, reducing hepatotoxicity risk.

Answer 16

- Is **least likely** to form carbon monoxide when exposed to carbon dioxide absorbents. - However, it breaks down to form toxic compounds in animals, **primarily** **compound A** - Although levels in humans are below speculated toxic levels even at low gas flows.

Answer 17

- Xenon is an inert gas - MAC of 63% to 71% - More potent than nitrous oxide. - It is nonexplosive, odorless, chemically inert, environmentally friendly - Has a blood:gas partition coefficient of 0.115.

Answer 18

- Xenon's high cost limits its use, though this could be offset by low fresh gas flow rates and xenon-recycling systems. - Its acceptance depends on demonstrating special properties or significantly lower morbidity - Mortality during anesthesia.

Answer 19

- Xenon can favor air bubble expansion, which may exacerbate neurologic injury from venous air embolism. - It has a minimal effect on bowel expansion compared to nitrous oxide.

Answer 20

- Is 2 to 3 times faster than from equal-MAC nitrous oxide plus isoflurane or sevoflurane. - Xenon is a potent hypnotic and analgesic without causing hemodynamic depression.

Answer 21

- Offers neuroprotection without psychotomimetic behavioral changes - It does not stimulate dopamine release from the nucleus accumbens, unlike ketamine or nitrous oxide.

Answer 22

- Indicates the ratio of end-tidal anesthetic concentration (FA) to inspired anesthetic concentration (FI) - Describes the uptake of inhaled anesthetics during induction. - It reflects how quickly the anesthetic reaches equilibrium in the lungs.

Answer 23

- Anesthetics with lower blood:gas partition coefficients have a more rapid increase in their FA/FI ratio compared to more soluble anesthetics, - Indicates faster pulmonary uptake and equilibrium. ## Footnote Lower blood:gas partition coefficients: nitrous oxide, desflurane, and sevoflurane

Answer 24

- Suggests decreased tissue uptake as vessel-rich group tissues become saturated with the anesthetic.

Answer 25

1. Absorption from alveoli to blood 2. Distribution in the body 3. Metabolism 4. Elimination (mainly via lungs)

Answer 26

- Aging leads to changes in body composition (less lean mass, more fat) - Affects the volume of distribution - It may also impair pulmonary gas exchange - Reduce cardiac output - Alter tissue perfusion and anesthetic distribution.

Answer 27

- A series of partial pressure gradients, starting at the anesthetic machine, move the anesthetic across alveoli, capillaries, and cell membranes to the CNS.

Answer 28

- The main goal is to achieve a constant and optimal brain partial pressure of the inhaled anesthetic, correlating with PA (alveolar partial pressure) and PBRAIN (brain partial pressure).

Answer 29

- Indicates the depth of anesthesia, recovery from anesthesia - Anesthetic equal potency (MAC) - It mirrors PBRAIN at a steady state - allows for control of anesthetic doses to the brain

Answer 30

- Equilibration means equal partial pressures in two phases, not equal concentrations. - This concept is key in controlling doses of volatile anesthetics.

Answer 31

The balance of input (delivery) into alveoli and uptake (loss) from alveoli into arterial blood. **Input depends on:** * The inhaled partial pressure (PI) * Alveolar ventilation * Characteristics of the anesthetic breathing system.

Answer 32

Anesthetic input into alveoli depends on: * The inhaled partial pressure (PI) of the anesthetic * The rate of alveolar ventilation * The design of the anesthetic delivery system

Answer 33

* The solubility of the anesthetic in body tissues * Cardiac output * The alveolar-to-venous partial pressure differences (A-vD)

Answer 34

* To offset anesthetic uptake accelerating anesthesia induction. * This quickens the rate of rise in the PA and PBRAIN. * As uptake decreases over time, PI should be reduced to maintain a constant and optimal PBRAIN.

Answer 35

* States that a higher PI leads to a more rapid increase in PA * As the higher concentration offsets uptake, speeding up the PA's rise. * It results from a concentrating effect and augmentation of tracheal inflow.

Answer 36

* Concentrating the anesthetic in a smaller lung volume due to gas uptake * while increased tracheal inflow fills the space produced by gas uptake

Answer 37

* Occurs when the high-volume uptake of a primary gas (first gas) accelerates the PA rise of a secondary gas (second gas) * It's due to increased tracheal inflow and concentration of the second gas in a reduced lung volume from the high-volume uptake of the first gas

Answer 38

* It's misleading to suggest that extra gas is routinely drawn into the lungs to compensate for lost lung volume. * Compensatory changes may include decreased expired ventilation or a decrease in lung volume, not just increased inspired ventilation.

Answer 39

* Accelerates the input of anesthetics, raising the PA more rapidly towards the PI. * speeds up anesthesia induction. * Hyperventilation can decrease cerebral blood flow (CBF), which might offset the increased anesthetic delivery to the brain.

Answer 40

* Reduces anesthetic input * Slows the establishment of the necessary PA and PBRAIN for anesthesia induction.

Answer 41

* A higher alveolar ventilation to FRC ratio leads to a faster rate of increase in PA. * Neonates have a higher ratio (about 5:1) compared to adults (1.5:1) * Results in quicker anesthesia induction in neonates due to their higher metabolic rate.

Answer 42

* Have a dose-dependent depressant effect on alveolar ventilation * Creates a negative feedback mechanism * Prevents excessive anesthesia depth during spontaneous breathing * Decrease anesthetic delivery when ventilation is reduced.

Answer 43

* Anesthetics redistribute from high-concentration tissues (like the brain) to low-concentration tissues (like skeletal muscles). * When brain concentration drops below a threshold, ventilation increases, raising anesthetic delivery to the lungs

Answer 44

* Mechanism against excessive anesthesia depth, which is present during spontaneous breathing * This is because mechanical ventilation maintains consistent anesthetic delivery regardless of the brain's anesthetic concentration. ## Footnote Mechanism against excessive anesthesia depth, which is present during spontaneous breathing, is lost during mechanical ventilation.

Answer 45

* Changes in alveolar ventilation influence the PA of soluble anesthetics (like halothane, and isoflurane) * More than poorly soluble ones (like nitrous oxide, desflurane, sevoflurane). * Poorly soluble anesthetics have a rapid PA increase regardless of ventilation changes due to limited uptake.

Answer 46

* **More blood-soluble anesthetics have greater uptake**; thus, increasing alveolar ventilation accelerates the PA's approach to the PI. * Conversely, **uptake of poorly soluble anesthetics is limited**, so their PA rises rapidly regardless of ventilation changes.

Answer 47

* Increased alveolar ventilation, likely increases the depth of anesthesia (PA) for more blood-soluble anesthetics. * Due to faster PA rise towards the PI.

Answer 48

* The system's volume (acting as a buffer). * Solubility of anesthetics in the system's materials. * Gas inflow rate from the anesthetic machine. * High gas inflow rates can negate the buffering effect of the system's volume.

Answer 49

* Slows the achievement of the target PA by acting as a buffer. * High gas inflow rates can counteract this buffering effect.

Answer 50

* Initially slows the PA's rate of increase. * At the end of anesthetic administration, the reverse gradient causes anesthetic elution, slowing the PA's rate of decrease.

Answer 51

Methoxyflurane

Answer 52

- Halothane - Enflurane - Isoflurane

Answer 53

- Nitrous Oxide - Desflurane - Sevoflurane - Xenon

Answer 54

* Is a distribution ratio that describes how an inhaled anesthetic distributes itself between two phases (like blood and gas) at equilibrium. * It indicates the concentration relationship of the anesthetic in these phases when their partial pressures are equal.

Answer 55

* Blood:gas partition coefficient of 0.5 means the concentration of the anesthetic in the blood is half that in alveolar gases when their partial pressures are equal. * It indicates the solubility and distribution of the anesthetic between blood and gas.

Answer 56

* A brain:blood partition coefficient of 2 means the concentration of anesthetic in the brain is twice that in the blood when their partial pressures are equal. * It shows the relative concentration of anesthetic in the brain versus blood.

Answer 57

* Partition coefficients are temperature-dependent. * The solubility of a gas in a liquid decreases as the temperature of the liquid increases.

Answer 58

* The rate of PA increase towards the PI is inversely related to the anesthetic's solubility in blood. * Highly soluble anesthetics like methoxyflurane require more anesthetic to be dissolved in blood for PA to equilibrate with PI, leading to slower induction.

Answer 59

* The technique involves delivering a higher PI than required for the maintenance of anesthesia to speed up induction. * Particularly with highly soluble anesthetics. * Sustained high PI can result in overdose.

Answer 60

* Low blood solubility means minimal anesthetic needs to be dissolved for equilibration. * Results in rapid PA increase. * Quicker onset of effects ( anesthesia induction).

Answer 61

* At concentrations of 60-70%, leads to unique effects when used with volatile anesthetics or in air-containing cavities.

Answer 62

Vary with individual differences in: * Water. * Lipid Protein content. * Hematocrit levels. For example, lower hematocrit or a recent fatty meal can affect the solubility of volatile anesthetics in blood.

Answer 63

* The solubility of certain anesthetics like halothane, enflurane, methoxyflurane, and isoflurane is about 18% less in neonates and the elderly. * For less soluble anesthetics like sevoflurane, there's no significant difference in solubility between neonates and adults.

Answer 64

* Determines the uptake of anesthetics into tissues. * The time needed for tissues to equilibrate with the arterial partial pressure of anesthetics (Pa).

Answer 65

* Is estimated by calculating a time constant, defined as the amount of inhaled anesthetic that can be dissolved in the tissue divided by tissue blood flow. * One time constant represents **63%** equilibration. * Three time constants equal **95%** equilibration.

Answer 66

* Usually requires 5 to 15 minutes, or about three time constants, depending on the anesthetic's blood solubility.

Answer 67

* Is based on its fat:blood partition coefficient * Assumed fat blood flow, is estimated to be 25 to 46 hours for three time constants.

Answer 68

* Fasting leads to the transport of fat to the liver * potentially increasing anesthetic uptake by the liver * modestly slowing the rate of increase in the alveolar partial pressure (PA) of a volatile anesthetic during induction.

Answer 69

- Are directly related to anesthetic requirements. - An anesthetic's MAC (Minimum Alveolar Concentration) can be estimated as 150 divided by the oil:gas partition coefficient.

Answer 70

* Divide 150 by the anesthetic's oil:gas partition coefficient. ## Footnote **150** is a constant representing the average product of oil:gas solubility and MAC for various anesthetics

Answer 71

For an anesthetic with an oil:gas partition coefficient of 100, the calculated MAC would be 1.5% (150 divided by 100).

Answer 72

Nitrous oxide has a high blood:gas partition coefficient (0.46) compared to nitrogen (0.014), allowing it to rapidly accumulate in air-filled cavities, increasing volume or pressure, potentially leading to damage.

Answer 73

* In compliant cavities (like intestinal gas or pneumothorax), nitrous oxide causes expansion. * In noncompliant cavities (like the middle ear or cerebral ventricles), it increases intracavitary pressure.

Answer 74

* Partial pressure of nitrous oxide. * Blood flow to the cavity. * The duration of nitrous oxide administration. * In high-flow areas, volume increases can be rapid.

Answer 75

* Diffuses into the middle ear faster than nitrogen leaves, potentially increasing ear pressure * Especially if the **Eustachian tube** is blocked * Leads to tympanic membrane rupture or serous otitis after anesthesia.

Answer 76

* Can rapidly increase the volume of intraocular gas bubbles, enough to compress the retinal artery. * Potentially cause visual loss, especially critical in the weeks following ocular surgery.

Answer 77

* Changes in blood-gas solubility, influenced by the priming solution and temperature. * The overall effect of hypothermic bypass and a crystalloid prime on solubility is about 2%

Answer 78

* Volatile anesthetics initiated take longer to equilibrate. * If the anesthetics are already present when the bypass begins, they may be diluted, potentially reducing anesthesia depth.

Answer 79

**Increased cardiac output:** * rapid uptake of anesthetic from the alveoli. * Slowing the increase in PA and anesthesia induction. **Decreased cardiac output:** * Speeds up PA increase due to less anesthetic uptake.

Answer 80

* While increased cardiac output hastens the equilibration of tissue anesthetic partial pressures with Pa, it actually lowers the Pa than if cardiac output were normal, due to increased anesthetic uptake.

Answer 81

* Changes in cardiac output significantly influence the PA rate of increase for soluble anesthetics * Have little effect on poorly soluble anesthetics like nitrous oxide, regardless of cardiac output variations.

Answer 82

* May depress cardiac output, leading to a positive feedback response where decreased output raises PA * Deepening anesthesia and further depressing cardiac function.

Answer 83

* Increases in cardiac output may not proportionally increase blood flow to all tissues. * Preferential perfusion of vessel-rich tissues can lead to a faster increase in PA than if the increased cardiac output were evenly distributed.

Answer 84

* Dilutes anesthetic partial pressure in blood from ventilated alveoli * Decrease Pa * Slows anesthesia induction. * It creates a gradient where PA underestimates Pa, similar to its effect on PaO2.

Answer 85

* A right-to-left shunt slows the rate of increase of Pa for poorly soluble anesthetics * Soluble anesthetics' uptake offsets the dilutional effects of shunted blood * Uptake of poorly soluble anesthetics is minimal.

Answer 86

The impact of solubility in the presence of a right-to-left shunt is opposite to that observed with changes in cardiac output and alveolar ventilation.

Answer 87

Left-to-right shunts (like arteriovenous fistulas) deliver blood with a higher anesthetic partial pressure to the lungs, offsetting the dilutional effects of a right-to-left shunt on Pa.

Answer 88

* **Right-to-left shunt** on slowing PA increase is maximal without a left-to-right shunt. * **Left-to-right shunts** can only offset right-to-left shunt effects if both types of shunts are present.

Answer 89

* The **A-vD reflects tissue uptake** of inhaled anesthetics. * It affects lung uptake by controlling the rate of increase of the mixed venous partial pressure of the anesthetic, influenced by tissue solubility, blood flow, and arterial-to-tissue pressure differences.

Answer 90

* Equilibrate rapidly with arterial anesthetic pressure (Pa) due to high blood flow and low mass. * After three time constants, venous blood pressure equilibrates with alveolar pressure (PA), decreasing anesthetic uptake.

Answer 91

* Skeletal muscles and fat, comprising a large body mass but receiving less cardiac output * Continue to take up anesthetics for an extended period, maintaining the A-vD and continuous uptake from the lungs.

Answer 92

* Is faster in neonates and infants due to greater cardiac output to these tissues and decreased solubility of anesthetics in their tissues. * Skeletal muscle mass is a smaller fraction of body weight in the very young.

Answer 93

1. Rapid washout from the brain 2. Low solubility in brain tissue 3. High cardiac output to the brain. ## Footnote The rate of decrease in the brain's partial pressure (PBRAIN) as reflected by the alveolar partial pressure (PA).

Answer 94

* Unlike induction, which can be accelerated by the concentration effect, recovery can't be sped up similarly since you can't administer less than zero. * Tissue concentrations at recovery's start depend on the anesthetic's solubility and administration duration.

Answer 95

Since some tissues (like skeletal muscles and fat) may not equilibrate with PA during maintenance, the PA decrease rate during recovery is faster than its increase rate during induction. These tissues continue taking up anesthetic, aiding PA decrease.

Answer 96

* Recovery time is **prolonged for soluble anesthetics** (like halothane, isoflurane) in proportion to anesthesia duration. * For **poorly soluble anesthetics** (like sevoflurane, desflurane), duration has **minimal impact on recovery time**

Answer 97

* Will pass back into the breathing circuit gases at anesthesia's end slowing the PA decrease rate. * Increasing fresh gas flow rates at conclusion can help mitigate rebreathing of exhaled anesthetics.

Answer 98

* Refers to the pharmacokinetics of the elimination of inhaled anesthetics, which depends on the duration of administration and the blood-gas solubility of the anesthetic. * It varies for different anesthetics and increases with the duration of anesthesia.

Answer 99

* Recovery is fastest with desflurane (most insoluble) and * Slowest with isoflurane (most soluble). * For short procedures (around 30 minutes), there's little difference in recovery time among these anesthetics. * The difference becomes appreciable in longer procedures.

Answer 100

In longer procedures (3-4 hours), turning off sevoflurane about 30 minutes before the end and replacing it with 70% nitrous oxide can ensure rapid recovery by allowing adequate time for a 90% decrease in sevoflurane concentration.

Answer 101

* The initial phase of elimination, primarily driven by alveolar ventilation, * Reflected in the 50% decrement time of various anesthetics, * which is typically less than 5 minutes and doesn’t increase much with anesthesia duration.

Answer 102

- Desflurane and sevoflurane have 80% decrement times under 8 minutes - Enflurane and isoflurane, these times increase after 60 minutes. - The 90% decrement time of desflurane increases slightly with longer anesthesia but remains significantly less than for other anesthetics after 6 hours.

Answer 103

* Occurs when nitrous oxide is abruptly discontinued * Causes it to rapidly leave the blood and enter the alveoli, diluting the PAO2 (alveolar oxygen partial pressure) * Potentially lowering the PaO2 (arterial oxygen partial pressure).

Answer 104

* Can dilute both PAO2 and PACO2 (alveolar carbon dioxide partial pressure). * Reduces the stimulus to breathe. * Exacerbates the decrease in PaO2.

Answer 105

* Administer oxygen to fill the lungs at the end of anesthesia, * It counteract the dilution of PAO2 by nitrous oxide.

Answer 106

* Is the concentration of an inhaled anesthetic at 1 atm that prevents movement in response to a painful stimulus in 50% of patients. * It's considered the anesthetic 50% effective dose (ED50) for immobility.

Answer 107

* The MAC primarily reflects the effects of inhaled anesthetics on the spinal cord, with a minor component resulting from cerebral effects.

Answer 108

* MAC provides a uniform measure of potency for inhaled anesthetics * allows for standardization of dosages * comparison of drugs * investigation into mechanisms of anesthetic action.

Answer 109

* MAC shows a remarkably small pharmacodynamic variability * Varying only 10-15% among individuals. * This consistency is unique in pharmacology.

Answer 110

* **MAC-awake** is the concentration of an anesthetic that prevents consciousness in 50% of patients, typically about half of the MAC. * **MAC-memory** is even lower, associated with amnesia in 50% of patients.

Answer 111

- Hyperthermia - Excess pheomelanin production (red hair) - Drug-induced increases in CNS catecholamines levels (cocaine, methamphetamines, amphetamines) - Cyclosporine * Hypernatremia

Answer 112

- Hypothermia - Increasing age - Preoperative medication - Drug-induced decreases in CNS catecholamine levels - Alpha2 Agonist - Acute ETOH ingestion - Pregnancy - Postpartum (returns to normal in 24-72 hr) - Lidocaine - Neuraxial opioids - PaO2 < 38 mmHg - MAP < 40 mmHg - Cardiopulmonary bypass

Answer 113

- Anesthetic metabolism - Chronic alcohol abuse - Sex - Duration of anesthesia - PaCo2 15-95 mmHg - PaO2 > 38 mmHg - BP > 40 mmHg - Hyperkalemia or Hypokalemia - Thyroid gland dysfunction

Answer 114

* Remarkably uniform in humans * Primarily influenced by age and body temperature.

Answer 115

* Increasing age leads to a progressive decrease in MAC, * With a **reduction of about 6% per decade** * Consistent across all inhaled anesthetics.

Answer 116

* MAC **decreases by nearly 30%** during pregnancy and the early postpartum period. * Returning to **normal within 12 to 72 hours** after childbirth.

Answer 117

* Despite a reduction in MAC during pregnancy, the incidence of postoperative awareness is higher. * Especially after cesarean sections. * This indicates that the concentration-response in the brain isn't significantly altered in pregnancy.

Answer 118

* Is required to induce EEG changes associated with hypnosis * Is not changed in pregnancy, indicating that brain response to anesthetic concentrations remains consistent.

Answer 119

* Gender does not influence MAC * Except in women with natural red hair who have increased MAC possibly due to mutations in the melanocortin-1 receptor gene.

Answer 120

The impact of cardiopulmonary bypass on MAC is uncertain, with studies showing either a decrease or no change.

Answer 121

* Cyclosporine **increases Isoflurane MAC** * Despite prolonging sleeping times in animals.

Answer 122

* MAC values may vary with different types of stimuli. * **Tracheal intubation** requires the highest MAC to prevent muscle responses, representing a more intense stimulus than surgical skin incision.

Answer 123

* Yes, the effects of inhaled anesthetics are additive. * For example, 0.5 MAC nitrous oxide plus 0.5 MAC isoflurane equals the effect of 1 MAC of either anesthetic alone.

Answer 124

* Opioids synergistically decrease anesthetic requirements. * Fentanyl reduces desflurane MAC by 48% to 68%, depending on the dose.

Answer 125

* Interactions are mostly synergistic, not additive. * Different receptor actions or mechanisms typically lead to synergism.

Answer 126

* Dose-response curves for inhaled anesthetics are steep. * A dose of 1 MAC prevents movement in response to a painful stimulus in 50% of patients. * 1.3 MAC prevents movement in at least 95% of patients.

Answer 127

* The exact mechanism of volatile anesthetic action remains unclear. * Unlike most drugs with known specific molecular binding sites, the mode of action for volatile anesthetics is still a significant mystery.

Answer 128

* Suggests that inhaled anesthetics act by disrupting nerve membrane structures or dynamics, with potency correlating with lipid solubility (oil:gas partition coefficient). * Anesthetics dissolve in lipid cell membranes, affecting ion channels and synaptic transmission.

Answer 129

* By dissolving in lipid membranes, altering their shape and function. * This theory is supported by the fact that high pressures can partially reverse anesthetic effects by compressing membranes back to their normal state.

Answer 130

**The theory's limitations include**: * the minimal effect of anesthetics on lipid bilayer fluidity. * the fact that not all lipid-soluble drugs are anesthetics. * Some lipid-soluble drugs, like certain n-alcohols, are actually convulsants.

Answer 131

Refined lipid theories suggest that specialized domains in membranes, particularly those surrounding proteins, are sensitive to anesthetics and crucial to membrane function. Anesthetic effects could be due to binding to proteins or dissolving in lipids.

Answer 132

* Stereoselectivity refers to the different effects of anesthetic isomers on neuronal channels. * For instance, isoflurane's levoisomer is more potent than its dextroisomer in enhancing potassium conductance in neurons and in anesthetic potency.

Answer 133

* The levoisomer of isoflurane is more potent than the dextroisomer, * both in enhancing neuronal potassium conductance and in overall anesthetic potency, as shown by differences in MAC in rats.

Answer 134

* Yes, some studies have not found significant differences in the effects of enantiomers of isoflurane and desflurane on anesthetic effects in animals, suggesting variability in stereoselectivity findings

Answer 135

Receptor specificity in anesthetics is indicated by changes in anesthetic effects when molecular volume is increased, even though lipid solubility also increases. However, molecular shape and size offer limited insight into the anesthetic binding site structure.

Answer 136

* **Ionotropic receptors**, or ligand-gated ion channels, directly bind neurotransmitters to open ion channels, affecting membrane potential. * They are often multi-subunit structures. * **Metabotropic receptors**, typically monomeric, activate G proteins upon neurotransmitter binding, influencing other signaling molecules.

Answer 137

Ionotropic receptors like GABAA and nicotinic acetylcholine receptors are made from various subunits that form pleomorphic receptors, adapting to different neurotransmitters and functions.

Answer 138

Metabotropic receptors, upon binding with neurotransmitters like acetylcholine, activate G proteins, which then function as second messengers to activate protein kinases or modulate potassium or calcium channels.

Answer 139

Inhaled anesthetics do not appear to stimulate endogenous opioid release, nor do they suppress ventilatory responses to surgical stimulation at movement-suppressing concentrations.

Answer 140

Small doses of opioids decrease MAC, indicating their ability to provide analgesic effects, which are absent in inhaled anesthetics alone.

Answer 141

Glycine receptors, primarily located in the spinal cord, are potentiated by volatile anesthetics and may mediate part of the immobility effect (as defined by MAC) produced by these anesthetics.

Answer 142

While GABAA receptors are potentiated by volatile anesthetics, their enhancement at clinical concentrations has minimal influence on MAC, suggesting they do not majorly mediate the immobility caused by inhaled anesthetics.

Answer 143

β3–subunit–containing GABAA receptors mediate hypnosis and part of the immobility produced by injected anesthetics like propofol and etomidate.

Answer 144

Inhaled anesthetics decrease excitatory neurotransmission, primarily mediated by glutamate, the main excitatory neurotransmitter in the mammalian CNS.

Answer 145

Glutamate receptors affected include G protein–coupled receptors and ligand-gated receptors such as NMDA, AMPA, and kainate. NMDA receptors, in particular, may mediate some behavioral effects of inhaled anesthetics.

Answer 146

At 1 MAC, volatile anesthetics inhibit NMDA receptors to varying degrees, ranging from 14% (sevoflurane) to 39% (Xenon). Anesthetics with cation-π interactions show greater NMDA blockade.

Answer 147

Two-pore potassium channels help maintain the cell's resting potential and respond to internal stimuli, such as changes in pH. They are intrinsic membrane receptor/ion channels.

Answer 148

Volatile anesthetics potentiate the activity of two-pore potassium channels, particularly TREK and TASK channels, in an agent-specific manner. These channels are sensitive to anesthetics at clinically used concentrations.

Answer 149

TASK-3 receptors, sensitive to anesthetics, play a role in maintaining theta oscillations in the EEG, which are associated with anesthesia and natural deep sleep durations

Answer 150

TASK channel interaction with anesthetics may contribute to neuroprotective effects during ischemia-reperfusion injury, a potential benefit of anesthetic intervention.

Answer 151

There are many subtypes of sodium channels, each playing different roles. Some subtypes, particularly those modulating neurotransmitter release, are more sensitive to anesthetics than those mediating axonal conduction.

Answer 152

Anesthetics interact with specific subtypes of sodium channels at presynaptic junctions, inhibiting the release of neurotransmitters like glutamate.

Answer 153

Intravenous administration of lidocaine, which nonspecifically blocks sodium channels, has been shown to decrease MAC, indicating the role of sodium channels in anesthetic potency.

Answer 154

These are voltage-gated ion channels crucial in regulating rhythmogenicity in the heart and brain, expressed throughout the body.

Answer 155

Halothane may influence these channels in motor neurons, potentially contributing to anesthetic immobility.

Answer 156

MAC represents the ability of inhaled anesthetics to induce immobility primarily through actions on the spinal cord, rather than higher brain centers. This is why immobility during noxious stimulation doesn't correlate with cortical EEG activity.

Answer 157

Inhaled anesthetics depress excitatory AMPA and NMDA receptor-mediated currents and potentially act on two-pore potassium channels, contributing to immobility. However, they do not significantly affect inhibitory GABAA or glycine receptors in this context.

Answer 158

No, nicotinic acetylcholine receptors do not significantly contribute to anesthetic-induced immobility at the spinal cord level.

Answer 159

While opioids and α2-adrenergic receptor stimulation (like clonidine) decrease MAC, they are unlikely to be the mechanisms by which inhaled anesthetics produce immobility. Inhaled anesthetics do not act via opioid receptors.

Answer 160

No single receptor group action can fully explain the immobility caused by inhaled anesthetics. It is unlikely that immobility results from concurrent actions on many different receptors.

Answer 161

The exact mechanism of anesthesia-induced unconsciousness is not fully understood. It is studied as the loss of righting reflex in animals and loss of response to command in humans, with distinct molecular targets potentially contributing to this state.

Answer 162

Hypnosis is typically measured as a loss of response to a command or through the spared arm technique in the presence of neuromuscular blockers. It indicates a state of unconsciousness separate from immobility and amnesia.

Answer 163

Clinical anesthesia may involve diminishing afferent sensory impulses (by drugs like opioids), depressing central activating systems (via benzodiazepines, barbiturates, propofol), and suppressing motor reflexes (by volatile anesthetics and others).

Answer 164

Volatile anesthetics are considered 'total anesthetics' because they can independently provide general anesthesia. They are effective in depressing motor reflexes, a key component of general anesthesia.

Answer 165

Certain inhaled anesthetics inhibit synaptic transmission by presynaptic inhibition of neurotransmitter release. This may involve actions on ion channels regulating neurotransmitter release or directly on the release machinery.

Answer 166

Isoflurane inhibits presynaptic neurotransmitter release, affecting the machinery required for the release process.

Answer 167

Inhaled anesthetics produce different pharmacologic effects even at comparable percentages of MAC, indicating that their dose-response curves are not parallel. This variation is observed in their effects on various organ systems.

Answer 168

Comparisons are based on measurements from normothermic volunteers under controlled ventilation and normocapnia, exposed to equal potent concentrations of inhaled anesthetics.

Answer 169

Surgically stimulated patients with various confounding variables may respond differently to inhaled anesthetics compared to the responses observed in healthy volunteers.

Answer 170

Desflurane and sevoflurane have lower blood and tissue solubility, allowing for more precise control during induction and faster recovery upon discontinuation. Their other properties mostly resemble those of their predecessors.

Answer 171

* Anesthetic concentration * Rate of increase in anesthetic concentration * Spontaneous versus controlled ventilation * Variations from normocapnia * Surgical stimulation * Patient age * Coexisting disease * Concomitant drug therapy * Intravascular fluid volume * Preoperative medication * Injected drugs to induce and/or maintain anesthesia or skeletal muscle relaxation * Alterations in body temperature

Answer 172

Mental impairment is not detectable in volunteers exposed to 0.16% nitrous oxide or 0.0016% halothane, suggesting that operating room personnel using modern anesthetic scavenging techniques are unlikely to experience mental impairment from trace anesthetic exposure.

Answer 173

Reaction times do not significantly increase until individuals inhale 10% to 20% nitrous oxide.

Answer 174

Cerebral metabolic oxygen requirements decrease in parallel with reductions in cerebral activity induced by anesthetics.

Answer 175

Drug-induced increases in cerebral blood flow (CBF) can lead to elevated intracranial pressure, particularly in patients with space-occupying lesions.

Answer 176

The effects of desflurane and sevoflurane on the CNS do not significantly differ from those of older inhaled anesthetics.

Answer 177

At concentrations below 0.4 MAC, volatile anesthetics increase EEG frequency and voltage, corresponding to the "excitement stage" of anesthesia.

Answer 178

- There is a shift of high-voltage activity from posterior to anterior brain regions - cerebral metabolic oxygen requirements decrease, - likely indicating a transition from wakefulness to unconsciousness.

Answer 179

- EEG frequency decreases - Voltage increases - During isoflurane administration, burst suppression appears at about 1.5 MAC, with electrical silence at 2 MAC.

Answer 180

* Electrical silence is not observed with enflurane * High concentrations (>3.5 MAC) of halothane are required for this effect. * Nitrous oxide produces slower frequency and higher voltage on the EEG, similar to volatile anesthetics.

Answer 181

Desflurane and sevoflurane cause dose-related changes in the EEG similar to isoflurane. Desflurane initially increases frequency and lowers voltage at low concentrations, with higher concentrations leading to increased voltage and electrical silence at 1.5 to 2.0 MAC.

Answer 182

Enflurane can induce EEG changes similar to seizures, especially at concentrations >2 MAC or with significant hyperventilation. It may cause tonic-clonic muscle twitching, but does not generally enhance preexisting seizure foci.

Answer 183

Isoflurane does not induce seizure activity on EEG, even under deep anesthesia or hypocapnia. It possesses anticonvulsant properties and can suppress seizures induced by other agents.

Answer 184

Desflurane and sevoflurane generally do not produce EEG evidence of convulsive activity, though there are reports of EEG seizure activity during sevoflurane anesthesia in certain individuals.

Answer 185

Nitrous oxide may increase motor activity and induce seizures, especially at high concentrations in hyperbaric settings. It may also be associated with withdrawal seizures and post-anesthesia delirium or excitement.

Answer 186

Withdrawal seizures can occur in animals after discontinuation of nitrous oxide, possibly reflecting acute dependence. Similar phenomena might occur in humans, manifesting as delirium or excitement during recovery.

Answer 187

Volatile anesthetics cause a dose-related decrease in amplitude and an increase in latency of cortical components of median nerve somatosensory, visual, and auditory evoked potentials, with amplitude decreases being more pronounced than latency increases.

Answer 188

Nitrous oxide, even on its own, can decrease the amplitude of cortical somatosensory evoked potentials. When combined with halothane, enflurane, or isoflurane, it allows for adequate waveform monitoring at specific MAC levels.

Answer 189

Adequate cortical somatosensory evoked potential waveforms can be monitored with 60% nitrous oxide during administration of 0.50 to 0.75 MAC halothane and 0.5 to 1.0 MAC enflurane and isoflurane.

Answer 190

Desflurane increasingly depresses somatosensory evoked potentials in patients at peri-MACs ranging from 0.5 to 1.5 MAC.

Answer 191

Inhaled anesthetics cause loss of response to verbal command at MAC-awake concentrations, which is typically a lower concentration than that required for full anesthesia.

Answer 192

Subtle effects on mental function, such as learning impairment, may occur at anesthetic concentrations as low as 0.2 MAC.

Answer 193

Gaseous anesthetics vary in their effectiveness to prevent awareness. For instance, 0.4 MAC isoflurane prevents recall and responses to commands, while nitrous oxide requires more than 0.5 to 0.6 MAC to achieve similar effects.

Answer 194

Surgical stimulation may increase the anesthetic requirement to prevent awareness, indicating a higher concentration of anesthetic may be needed during active surgical procedures.

Answer 195

Volatile anesthetics produce dose-dependent increases in CBF, which occurs despite decreases in cerebral metabolism. The magnitude of CBF increase depends on the balance between the drug's vasodilatory actions and flow-metabolism coupling.

Answer 196

Sevoflurane has a dose-dependent cerebral vasodilatory effect, less than that of isoflurane. Both desflurane and isoflurane are similar in increasing CBF and maintaining reactivity to carbon dioxide.

Answer 197

Nitrous oxide increases CBF, potentially more potently than an equipotent dose of isoflurane. However, its use at concentrations <1 MAC limits the magnitude of this change.

Answer 198

In animals, halothane-induced increases in CBF return to baseline levels over time, starting after about 30 minutes and normalizing after about 150 minutes. This normalization is not seen in patients during surgery, where CBF remains increased.

Answer 199

Isoflurane retains CBF autoregulation in response to changes in systemic blood pressure at 1 MAC, unlike halothane. Desflurane and sevoflurane do not significantly alter CBF autoregulation, with cerebrovascular carbon dioxide reactivity being largely intact.

Answer 200

Inhaled anesthetics produce dose-dependent decreases in cerebral metabolic oxygen requirements. Isoflurane leads to a greater decrease than an equivalent MAC of halothane.

Answer 201

Once the EEG is isoelectric, increasing the concentration of volatile anesthetics further does not produce additional decreases in cerebral metabolic oxygen requirements.

Answer 202

Isoflurane's greater decrease in cerebral metabolism means less CO2 production, which can oppose increases in CBF. Unexpected increases in CBF might occur if isoflurane is administered to patients whose cerebral metabolism is already decreased by other drugs.

Answer 203

Desflurane and sevoflurane decrease cerebral metabolic oxygen requirements in a manner similar to isoflurane.

Answer 204

Neurologic outcomes are generally not different based on the type of volatile anesthetic used. However, data suggest that isoflurane may offer some degree of cerebral protection compared to enflurane and halothane.

Answer 205

Isoflurane may blunt necrotic processes resulting from cerebral ischemia, particularly in procedures like carotid endarterectomy. Additionally, during controlled hypotension for cerebral aneurysm clipping, isoflurane can favorably alter the global cerebral oxygen supply-demand balance.

Answer 206

Inhaled anesthetics increase ICP, with this increase paralleling the rise in cerebral blood flow (CBF). Patients with intracranial masses are especially susceptible to these ICP increases.

Answer 207

In hypocapnic humans with intracranial masses, desflurane at concentrations <0.8 MAC does not increase ICP, while 1.1 MAC can increase ICP by about 7 mm Hg.

Answer 208

Hyperventilation, reducing PaCO2 to about 30 mm Hg, can oppose the tendency of inhaled anesthetics to increase ICP.

Answer 209

With enflurane, hyperventilation increases the risk of seizure activity, which can lead to increased cerebral metabolism and CO2 production, potentially increasing CBF and ICP.

Answer 210

The ability of nitrous oxide to increase ICP is probably less than that of volatile anesthetics, partly due to its restricted dose of <1 MAC.

Answer 211

Isoflurane does not alter the production of CSF but decreases the resistance to its reabsorption. This aligns with the minimal increases in ICP observed during isoflurane administration.

Answer 212

Increases in ICP associated with nitrous oxide are presumed to be due to increases in CBF. Nitrous oxide does not enhance CSF production.

Answer 213

Inhaled anesthetics produce dose-dependent and drug-specific effects on the circulatory system, including changes in blood pressure, heart rate, cardiac output, stroke volume, right atrial pressure, systemic vascular resistance, cardiac rhythm, and coronary blood flow.

Answer 214

Desflurane's circulatory effects are similar to isoflurane, while sevoflurane shares characteristics with both isoflurane and halothane.

Answer 215

Circulatory responses can vary with controlled versus spontaneous breathing, preexisting cardiac disease, and the presence of drugs affecting the heart.

Answer 216

The circulatory effects often reflect inhaled anesthetics' influence on myocardial contractility, peripheral vascular smooth muscle tone, and autonomic nervous system activity.

Answer 217

These anesthetics produce similar, dose-dependent decreases in mean arterial pressure in healthy volunteers, with the magnitude of decrease being greater than during surgical stimulation.

Answer 218

Artificially elevated preoperative blood pressure levels, possibly due to apprehension, may result in greater decreases in blood pressure than the actual pharmacologic effect of the volatile anesthetic.

Answer 219

Nitrous oxide generally causes no change or modest increases in systemic blood pressure. Substituting nitrous oxide for a portion of volatile anesthetic decreases the extent of blood pressure decrease caused by the anesthetic alone.

Answer 220

The blood pressure decrease with halothane is partly due to reductions in myocardial contractility and cardiac output, while with isoflurane, desflurane, and sevoflurane, it primarily results from decreased systemic vascular resistance.

Answer 221

Isoflurane and desflurane tend to increase heart rate at lower concentrations, whereas sevoflurane increases heart rate only at concentrations >1.5 MAC. Halothane does not increase heart rate.

Answer 222

Heart rate effects in surgical patients can differ significantly from those in volunteers due to confounding variables like surgical stress, preoperative medication, and sympathetic nervous system activity.

Answer 223

A small dose of opioid premedication can prevent the heart rate increase commonly associated with isoflurane and possibly other volatile anesthetics.

Answer 224

Halothane may lead to an unchanged or decreased heart rate despite a drop in blood pressure, likely due to suppression of the sinus node and carotid sinus baroreceptor reflex response. It can also cause junctional rhythm and slow cardiac impulse conduction.

Answer 225

Heart rate responses to isoflurane are blunted in elderly patients, while younger patients are more likely to experience increased heart rates, especially in the presence of drugs with vagolytic effects.

Answer 226

Halothane produces dose-dependent decreases in cardiac output in healthy human volunteers. Its effect on cardiac output is more pronounced than other volatile anesthetics.

Answer 227

Isoflurane, desflurane, and sevoflurane do not significantly decrease cardiac output. Sevoflurane decreases cardiac output only at higher concentrations but recovers near awake values at 2 MAC.

Answer 228

Despite differences in heart rate effects, all volatile anesthetics decrease left ventricular stroke volume by 15% to 30%.

Answer 229

Nitrous oxide modestly increases cardiac output, likely due to its mild sympathomimetic effects.

Answer 230

Volatile anesthetics depress myocardial contractility in vitro. However, the vasodilating effects of ether-derivative anesthetics make their myocardial depression less apparent than halothane's. Nitrous oxide's myocardial depressant effects are milder and often offset by its sympathomimetic properties.

Answer 231

Halothane, isoflurane, and desflurane increase right atrial pressure (central venous pressure) in healthy volunteers, with minimal changes at 1 MAC. Sevoflurane, however, does not significantly affect right atrial pressure.

Answer 232

The peripheral vasodilating effects of volatile anesthetics tend to minimize the impact of their direct myocardial depression on right atrial pressure.

Answer 233

Nitrous oxide can increase right atrial pressure, likely due to increased pulmonary vascular resistance from its sympathomimetic effects.

Answer 234

Isoflurane, desflurane, and sevoflurane decrease systemic vascular resistance, leading to a decrease in blood pressure primarily through vasodilation. Halothane, however, does not change systemic vascular resistance significantly.

Answer 235

Halothane decreases systemic blood pressure mainly by reducing cardiac output, not by changing systemic vascular resistance.

Answer 236

Nitrous oxide does not significantly change systemic vascular resistance.

Answer 237

Isoflurane significantly increases skeletal muscle and cutaneous blood flow, which can lead to excessive perfusion, loss of body heat, and enhanced drug delivery to areas like the neuromuscular junction.

Answer 238

While halothane is a potent cerebral and cutaneous vasodilator, its effects are balanced by unchanged or constricted blood flow in other vascular beds, resulting in an overall unchanged systemic vascular resistance.

Answer 239

All volatile anesthetics increase cutaneous blood flow, which can arterialize peripheral venous blood. This effect can provide an alternative means of evaluating pH and PaCO2 without needing arterial blood samples.

Answer 240

The increase in cutaneous blood flow most likely results from a central inhibitory action of volatile anesthetics on temperature-regulating mechanisms.

Answer 241

Volatile anesthetics generally have little or no predictable effect on pulmonary vascular smooth muscle, meaning they don't significantly alter pulmonary vascular resistance

Answer 242

Nitrous oxide can increase pulmonary vascular resistance, which is especially pronounced in patients with existing pulmonary hypertension or in neonates.

Answer 243

In patients with congenital heart disease, the increase in pulmonary vascular resistance due to nitrous oxide may exacerbate right-to-left intracardiac shunting, worsening arterial oxygenation.

Answer 244

Halothane, an alkane derivative, greatly increases the sensitivity to epinephrine-induced ventricular dysrhythmias. In contrast, ether derivatives like isoflurane, desflurane, and sevoflurane have minimal to no effect in increasing this susceptibility.

Answer 245

Halothane, enflurane, and isoflurane can prolong the QTc interval on the electrocardiogram in healthy patients. Sevoflurane has also been reported to prolong the QTc interval, especially in patients with long QTc syndrome.

Answer 246

Generalizations from healthy patients may not be valid for those with idiopathic long QTc syndrome. Sevoflurane, in particular, has been noted to prolong the QT interval in these patients.

Answer 247

Sevoflurane can prolong the QTc interval in healthy patients, unlike propofol, which does not have this effect.

Answer 248

Most anesthetic agents, including volatile anesthetics, tend to suppress these arrhythmias by reducing adrenergic tone. Volatile anesthetics are preferred for minimal interference.

Answer 249

Propofol can suppress ectopic atrial tachycardia in children and may be used to control electrical storm. It does not generally inhibit other arrhythmias.

Answer 250

Ketamine does not inhibit arrhythmias. It does not alter sinoatrial or atrioventricular node function but can stimulate hemodynamics through adrenergic stimulation.

Answer 251

During spontaneous breathing, volatile anesthetics lead to increased systemic blood pressure and heart rate, and decreased systemic vascular resistance, due to sympathetic stimulation from CO2 accumulation and improved venous return.

Answer 252

Accumulation of CO2 during spontaneous breathing can stimulate the sympathetic nervous system (respiratory acidosis) and might directly relax peripheral vascular smooth muscle, affecting circulatory dynamics.

Answer 253

Under spontaneous breathing, volatile anesthetics increase blood pressure and heart rate, with lower systemic vascular resistance, compared to controlled ventilation which maintains normocapnia.

Answer 254

They induce coronary vasodilation, acting preferentially on vessels with diameters of 20 to 50 microns.

Answer 255

Isoflurane acts on larger coronary vessels (20-50 microns), while adenosine also affects small precapillary arterioles.

Answer 256

Although volatile anesthetics could theoretically cause coronary steal syndrome by redistributing blood from ischemic to nonischemic areas, this effect is not clinically significant.

Answer 257

Yes, volatile anesthetics, including isoflurane, are considered cardioprotective despite concerns about coronary steal syndrome.

Answer 258

Abrupt increases in desflurane concentration can transiently increase mean arterial pressure and heart rate due to sympathetic nervous system and renin-angiotensin activity stimulation.

Answer 259

Both cause transient increases in blood pressure and heart rate, but desflurane induces significantly greater responses.

Answer 260

No, abrupt increases in the delivered concentration of sevoflurane do not trigger neurocirculatory responses.

Answer 261

- Fentanyl (1.5-4.5 μg/kg IV administered 5 minutes before the abrupt increase in desflurane concentration) - Esmolol (0.75 mg/kg IV 1.5 minutes before) - Clonidine (4.3 μg/kg orally 90 minutes before) - can blunt these responses. - Fentanyl is particularly effective due to minimal cardiovascular depressant effects and less postanesthetic sedation.

Answer 262

Alfentanil can blunt hemodynamic responses to an abrupt increase in desflurane concentration, but it does not predictably prevent the increase in plasma norepinephrine concentrations.

Answer 263

It may exacerbate myocardial depression, especially in cases with already compromised cardiac muscle contractility.

Answer 264

It can evoke neurocirculatory responses that are detrimental in coronary artery disease, potentially exacerbating the condition.

Answer 265

It may cause myocardial depression in these patients, a response not seen in individuals without heart disease.

Answer 266

Peripheral vasodilation from isoflurane can be harmful in aortic stenosis but beneficial in mitral/aortic regurgitation.

Answer 267

Drugs that alter sympathetic nervous activity, like antihypertensives or β-blockers, can modify the circulatory effects of anesthetics.

Answer 268

They decrease myocardial contractility, making the heart more susceptible to the depressant effects of anesthetics.

Answer 269

Mechanisms include direct myocardial depression, inhibition of CNS sympathetic activity, peripheral autonomic ganglion blockade, attenuated carotid sinus reflex activity, decreased cyclic AMP formation, reduced catecholamine release, and decreased calcium ion influx.

Answer 270

Isoflurane may exhibit mild β-adrenergic agonist properties, contributing to maintained cardiac output, increased heart rate, and decreased systemic vascular resistance.

Answer 271

Rapid increases in desflurane lead to a significant blood pressure rise, accompanied by increased plasma epinephrine, suggesting enhanced adrenal gland activity.

Answer 272

Nitrous oxide can cause increased plasma catecholamine levels, mydriasis, body temperature rise, diaphoresis, elevated right atrial pressure, and systemic and pulmonary vasoconstriction.

Answer 273

Opioids can mask nitrous oxide's sympathomimetic effects, revealing its direct depressant impact on the heart, characterized by lower blood pressure and cardiac output, and higher left ventricular end-diastolic pressure and systemic vascular resistance.

Answer 274

Ischemic preconditioning refers to brief episodes of myocardial ischemia that occur before a longer period of ischemia, offering protection against myocardial dysfunction and necrosis. This phenomenon involves complex interactions between myocardial organelles and various cells including neurons and lymphocytes. It highlights a protective mechanism that can be targeted for cardiac protection and is also observed in other organs like kidneys.

Answer 275

Inhaled anesthetics affect ventilation in several dose-dependent and drug-specific ways: - They alter the pattern of breathing. - They modulate the ventilatory response to carbon dioxide. - They affect the ventilatory response to arterial hypoxemia. - They influence airway resistance. Additionally, PaO2 (partial pressure of arterial oxygen) typically decreases during the administration of inhaled anesthetics if supplemental oxygen is not provided.

Answer 276

Except for isoflurane at >1 MAC, inhaled anesthetics cause a dose-dependent increase in the frequency of breathing. This is thought to be due to CNS stimulation. Isoflurane increases breathing frequency up to 1 MAC but not beyond. Nitrous oxide significantly increases breathing frequency at >1 MAC.

Answer 277

Isoflurane increases breathing frequency similarly to other anesthetics up to 1 MAC, but not beyond. Nitrous oxide, particularly at concentrations >1 MAC, increases breathing frequency more than other anesthetics and may stimulate pulmonary stretch receptors.

Answer 278

Volatile anesthetics likely stimulate central respiratory chemoreceptor neurons through the activation of THIK-1 receptors, responsible for a background potassium current, influencing breathing frequency.

Answer 279

Tidal volume decreases with anesthetic-induced increases in breathing frequency, leading to a rapid and shallow breathing pattern. This decrease in tidal volume results in reduced minute ventilation and increased PaCO2.

Answer 280

During general anesthesia, the breathing pattern becomes regular and rhythmic, contrasting the awake pattern of intermittent deep breaths. This change is characterized by rapid, shallow breaths due to the effects of inhaled anesthetics.

Answer 281

Volatile anesthetics cause a dose-dependent depression of ventilation, leading to decreased responsiveness to carbon dioxide and increased PaCO2 levels.

Answer 282

Desflurane and sevoflurane depress ventilation, causing profound decreases that can lead to apnea between 1.5 and 2.0 MAC. They both increase PaCO2 and reduce the ventilatory response to carbon dioxide.

Answer 283

COPD may increase the magnitude of PaCO2 when volatile anesthetics are used, accentuating ventilatory depression.

Answer 284

Nitrous oxide does not increase PaCO2. When combined with volatile anesthetics, it results in less depression of ventilation and a smaller increase in PaCO2 compared to volatile anesthetics alone.

Answer 285

All inhaled anesthetics, including nitrous oxide, decrease the slope of the carbon dioxide response curve and shift it to the right. Subanesthetic levels (0.1 MAC) do not alter the ventilatory response to carbon dioxide

Answer 286

Painful stimulation (such as surgical skin incision) and the duration of anesthetic administration can significantly affect the increase in PaCO2 produced by volatile anesthetics.

Answer 287

- Increases minute ventilation by approximately 40% due to rises in both tidal volume and frequency of breathing - PaCO2 decreases by only about 10% (4-6 mm Hg) despite this increase in minute ventilation. - This is thought to be due to heightened carbon dioxide production from sympathetic nervous system activation in response to the pain of surgical stimulation, which offsets the effects of increased minute ventilation.

Answer 288

- Volatile anesthetics like Desflurane and Sevoflurane lead to a dose-dependent depression of ventilation - characterized by reduced ventilatory response to carbon dioxide and increased PaCO2. - They can cause significant decreases in ventilation, leading to apnea at concentrations between 1.5 and 2.0 MAC. - Nitrous Oxide does not have this effect. - Nitrous Oxide combined with a volatile anesthetic is less depressing on ventilation and PaCO2 than the volatile anesthetic alone. - This suggests a ventilatory depressant–sparing effect of Nitrous Oxide detectable across all volatile anesthetics.

Answer 289

- After approximately 5 hours of administering a volatile anesthetic, the increase in PaCO2 produced by spontaneous breathing is less than that observed during the first hour of administration. - Additionally, the slope and position of the carbon dioxide response curve return to normal after about 5 hours of administering volatile anesthetics. - The reason for this apparent recovery from the ventilatory depressant effects of volatile anesthetics over time is not fully understood.

Answer 290

- Surgical stimulation can cause an approximate 40% increase in minute ventilation due to increases in both tidal volume and frequency of breathing. - PaCO2 only decreases by about 10% (4-6 mm Hg) despite the larger increase in minute ventilation. - This discrepancy is speculated to be due to the increased carbon dioxide production resulting from the activation of the sympathetic nervous system in response to painful surgical stimulation, which counteracts the effects of increased minute ventilation on PaCO2.

Answer 291

- Most commonly managed through the initiation of mechanical (controlled) ventilation of the patient's lungs. - The inherent ventilatory depressant properties of these anesthetics actually facilitate the transition to controlled ventilation - Making this an effective strategy for managing respiratory depression during anesthesia.

Answer 292

They profoundly depress this response. At 0.1 MAC, they cause 50%-70% depression, while 1.1 MAC leads to 100% depression.

Answer 293

They cause less significant depression of the ventilatory response to CO2 than to hypoxemia, especially at 0.1 MAC.

Answer 294

Inhaled anesthetics attenuate this usual synergistic effect, reducing the stimulation of ventilation.

Answer 295

No, sevoflurane-induced decreases in hypoxic responses are similar in both men and women.

Answer 296

Sevoflurane is a potent bronchodilator with low blood-gas solubility, allowing rapid anesthesia depth adjustment, and minimal effects on hypoxic pulmonary vasoconstriction.

Answer 297

Young age (<10 years), perioperative respiratory infection, endotracheal intubation, and presence of COPD.

Answer 298

Both anesthetics produce bronchodilation in COPD patients, with sevoflurane causing moderate bronchodilation.

Answer 299

Desflurane can induce bronchoconstriction, particularly in patients who smoke.

Answer 300

Administering fentanyl or morphine prior to desflurane induction significantly decreases airway irritability.

Answer 301

Sevoflurane is more effective than desflurane at suppressing moderate to severe cough responses.

Answer 302

Exposure to these absorbents can produce toxic gases, leading to airway irritation and impaired gas exchange, notably from formaldehyde generation.

Answer 303

- Originated in the 1960s. - Initially thought to increase tolerance to cerebral ischemia. - Positive associations in early studies, but not confirmed in high-quality, prospective studies.

Answer 304

- Suggests brief ischemia episodes can protect against longer ischemic periods. - Demonstrated in other organs like kidneys. - Brought forth by early anesthetic studies.

Answer 305

- Supported by animal studies, especially at extreme ages. - Associated with neuronal, glial apoptosis, and calcium dysregulation. - Potential postoperative cognitive effects in the elderly.

Answer 306

- May lead to postoperative delirium. - Postoperative cognitive dysfunction in 20%-40% of patients over 60.

Answer 307

- Early exposure linked to neurodegeneration and learning deficits in animal studies. - Concerns over prolonged exposure from observational studies. - FDA warning on anesthesia and brain development

Answer 308

- Studies the impact of anesthetic exposure on young children's brain development. - Concerns over multiple, prolonged anesthesia exposures.

Answer 309

- Isoflurane maintains total hepatic and hepatic artery blood flow. - Increases portal vein blood flow. - Acts as a vasodilator, enhancing hepatic oxygen delivery.

Answer 310

- Halothane acts as a vasoconstrictor. - Isoflurane increases hepatic blood flow and venous oxygen saturation. - Halothane does not change hepatic blood flow under similar conditions.

Answer 311

- Both maintain hepatic blood flow similar to isoflurane. - Contributes to maintaining hepatic oxygen delivery.

Answer 312

- Crucial for preventing postoperative hepatic dysfunction. - Hepatocyte hypoxia is a key factor in hepatic dysfunction etiology.

Answer 313

- They can decrease the intrinsic hepatic metabolism of certain drugs (e.g., propranolol) by 54-68%. - This is mainly due to anesthetic-induced inhibition of hepatic drug-metabolizing enzymes.

Answer 314

- Desflurane can cause transient increases in plasma alanine aminotransferase activity. - Both isoflurane and desflurane may lead to temporary rises in α-glutathione transferase, indicating hepatocellular injury. - Surgical stimulation, regardless of the anesthetic, can transiently impact hepatic function, evident in changes like bromsulphalein retention and liver enzyme elevation.

Answer 315

- Halothane is most notably associated with postoperative liver dysfunction, often linked to its metabolism and subsequent free radical production. - These free radicals can alter hepatic proteins, potentially creating antigens that trigger immune responses. - Preexisting liver conditions like hepatic cirrhosis are at higher risk, as anesthetics can further reduce hepatic oxygenation. - Hypothermia during surgery may protect the liver by reducing hepatic oxygen demand and mitigating the impact of anesthetics.

Answer 316

- Mild, self-limited postoperative hepatotoxicity: Occurs in ~20% of adults, marked by nausea, lethargy, fever, and minor liver enzyme increases. Likely related to hepatic blood flow changes impairing oxygenation. - Halothane hepatitis: Rarer, severe form, affecting 1 in 10,000 to 30,000 adults. Can lead to massive hepatic necrosis and death. Believed to be immune-mediated. Children are less susceptible.

Answer 317

- Manifestations: Eosinophilia, fever, rash, arthralgia, previous halothane exposure. - Risk Factors: Female gender, middle age, obesity, multiple halothane exposures. - Mechanism: Immune-mediated; antibodies against liver proteins modified by halothane metabolites. Histology: Acute hepatitis; genetic susceptibility suggested.

Chapter 4: Stoelting Inhaled Anesthetics Flashcards

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