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AAA-ANESTHESIOLOGY > INHALATIONAL ANESTHESIA > Flashcards

INHALATIONAL ANESTHESIA Flashcards

1
Q

What is general anesthesia characterized by?

A

Reversible loss of consciousness, analgesia, amnesia, and some degree of muscle relaxation.

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2
Q

Which substances are capable of producing general anesthesia?

A

Inert elements (xenon), simple inorganic compounds (nitrous oxide), halogenated hydrocarbons (halothane), ethers (isoflurane, sevoflurane, desflurane), and complex organic structures (propofol).

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3
Q

What receptors do nitrous oxide and xenon inhibit?

A

N-methyl-D-aspartate (NMDA) receptors.

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4
Q

What effects are mediated by gamma-aminobutyric acid (GABA) receptors in anesthesia?

A

Anesthetic effects through enhanced chloride channel conductance and inhibition in the CNS.

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5
Q

Which brain areas are affected by anesthetics?

A

Reticular activating system, cerebral cortex, cuneate nucleus, olfactory cortex, hippocampus, and the spinal cord.

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6
Q

What is the significance of cortical and subcortical anesthetic action?

A

Unconsciousness and amnesia are mediated by cortical action, while suppression of pain-related withdrawal is related to subcortical structures like the spinal cord and brain stem.

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7
Q

Where does MAC measurement suggest anesthetic effects occur?

A

Primarily at the spinal cord rather than the cerebral cortex.

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8
Q

What is the Meyer–Overton rule?

A

Anesthetic potency of inhalation agents correlates with their lipid solubility.

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9
Q

What does the critical volume hypothesis propose?

A

Anesthetics expand the lipid bilayer of membranes, altering their function.

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10
Q

What reverses anesthesia as proposed by the critical volume hypothesis?

A

Increased hydrostatic pressure.

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11
Q

How do inhalational agents modulate GABA receptors?

A

By binding to hydrophobic domains in GABA channel proteins, enhancing their inhibitory activity.

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12
Q

What other ion channels may play a role in anesthetic action?

A

Glycine receptors, nicotinic acetylcholine receptors, and NMDA receptors.

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13
Q

What concern is raised about general anesthetics in children?

A

Early exposure may promote cognitive impairment or neuronal apoptosis.

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14
Q

Which inhalational agent is linked to apoptosis in animal studies?

A

Isoflurane.

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15
Q

What is the role of xenon in neuroprotection?

A

It inhibits calcium influx after cell injury, reducing apoptosis.

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16
Q

What is the minimum alveolar concentration (MAC)?

A

The alveolar concentration that prevents movement in 50% of patients in response to a stimulus.

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17
Q

How does MAC relate to potency comparisons between anesthetic agents?

A

It mirrors brain partial pressure, allowing standardized potency comparisons.

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18
Q

How do MAC values of different anesthetics interact?

A

MAC values are roughly additive, e.g., 0.5 MAC nitrous oxide + 0.5 MAC halothane = 1.0 MAC.

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19
Q

How is MAC altered with aging?

A

MAC decreases by about 6% per decade of age.

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20
Q

What does 1.3 MAC represent clinically?

A

It prevents movement in approximately 95% of patients (similar to ED95).

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21
Q

What factors do not affect MAC?

A

Species, sex, and duration of anesthesia.

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22
Q

Where is the hypothesized site of motor inhibition by anesthetics?

A

The spinal cord, as MAC is unaffected by spinal cord transection in rats.

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23
Q

What is ischemic preconditioning?

A

A brief ischemic event protects cells from future ischemic injury.

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24
Q

What cardiac channel is involved in anesthetic preconditioning?

A

ATP-sensitive potassium (KATP) channels.

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25
Q

Which markers indicate myocardial protection by sevoflurane?

A

Reduced levels of troponin T.

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26
Q

Which volatile anesthetics have been linked to both neurotoxicity and neuroprotection?

A

Isoflurane and sevoflurane.

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27
Q

How does reactive oxygen species (ROS) relate to anesthetic injury?

A

ROS are associated with cellular damage, which anesthetics like xenon may reduce by inhibiting calcium influx.

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28
Q

How is MAC useful for experimental evaluations?

A

It provides a standard for comparing anesthetic effects and potencies.

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29
Q

At what MAC is awakening from anesthesia likely to occur?

A

0.3–0.4 MAC for most inhaled agents.

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30
Q

What are the physical properties of nitrous oxide?

A

Nitrous oxide is colorless, essentially odorless, nonflammable, and stored as a liquid under pressure because its critical temperature is above room temperature.

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31
Q

What receptor does nitrous oxide antagonize?

A

N-methyl-D-aspartate (NMDA) receptor.

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32
Q

How does nitrous oxide affect the cardiovascular system?

A

It stimulates the sympathetic nervous system, slightly increasing blood pressure, cardiac output, and heart rate in vivo, despite direct myocardial depression in vitro.

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33
Q

What is the effect of nitrous oxide on pulmonary vascular resistance?

A

Nitrous oxide increases pulmonary vascular resistance and modestly elevates right ventricular end-diastolic pressure.

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34
Q

How does nitrous oxide affect respiratory function?

A

It increases respiratory rate (tachypnea) and decreases tidal volume, with minimal change in minute ventilation and arterial CO2 levels.

35
Q

Why is hypoxic drive a concern with nitrous oxide use?

A

Nitrous oxide markedly depresses hypoxic drive, even at small concentrations.

36
Q

What are the cerebral effects of nitrous oxide?

A

It increases cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and intracranial pressure.

37
Q

Does nitrous oxide provide muscle relaxation?

A

No, nitrous oxide does not provide significant muscle relaxation and may cause skeletal muscle rigidity at high concentrations.

38
Q

How does nitrous oxide affect renal function?

A

Nitrous oxide decreases renal blood flow, glomerular filtration rate, and urinary output.

39
Q

What is the primary route of nitrous oxide elimination?

A

Almost all nitrous oxide is eliminated via exhalation.

40
Q

What is a potential toxicity of nitrous oxide related to vitamin B12?

A

Nitrous oxide irreversibly oxidizes the cobalt atom in vitamin B12, inhibiting methionine synthetase and thymidylate synthetase, potentially causing megaloblastic anemia and peripheral neuropathy.

41
Q

Why is nitrous oxide often avoided in early pregnancy?

A

Nitrous oxide may have teratogenic effects and is avoided in pregnant patients not in the third trimester.

42
Q

What is a contraindication for nitrous oxide related to air-containing cavities?

A

Nitrous oxide rapidly diffuses into air-containing cavities, such as pneumothorax or intracranial air, causing expansion and increased pressure.

43
Q

What is a significant drug interaction of nitrous oxide with volatile agents?

A

Nitrous oxide decreases the MAC of volatile agents by approximately 50%.

44
Q

What is a major environmental concern with nitrous oxide?

A

Nitrous oxide is an ozone-depleting gas with greenhouse effects.

45
Q

What are the physical properties of halothane?

A

Halothane is a halogenated alkane, nonflammable, and stabilized with thymol preservative in amber-colored bottles.

46
Q

How does halothane affect the cardiovascular system?

A

Halothane reduces arterial blood pressure and cardiac output dose-dependently and sensitizes the heart to arrhythmogenic effects of epinephrine.

47
Q

What are the respiratory effects of halothane?

A

Halothane causes rapid, shallow breathing, decreases tidal volume, and elevates resting PaCO2 levels. It also acts as a potent bronchodilator.

48
Q

How does halothane affect cerebral blood flow and intracranial pressure?

A

Halothane dilates cerebral vessels, increasing cerebral blood flow and intracranial pressure, though hyperventilation can prevent these rises.

49
Q

Is halothane a triggering agent for malignant hyperthermia?

A

Yes, halothane can trigger malignant hyperthermia.

50
Q

How does halothane affect renal function?

A

Halothane reduces renal blood flow, glomerular filtration rate, and urinary output.

51
Q

What are the hepatic effects of halothane?

A

Halothane decreases hepatic blood flow and can impair drug metabolism and clearance. It is also associated with rare cases of halothane hepatitis.

52
Q

What is the mechanism of halothane metabolism?

A

Halothane is oxidized in the liver to trifluoroacetic acid, with minor reductive metabolites under hypoxic conditions.

53
Q

What patients are at increased risk for halothane hepatitis?

A

Middle-aged obese women, those exposed to multiple halothane anesthetics, and individuals with familial predisposition to halothane toxicity.

54
Q

What are contraindications for halothane use?

A

Unexplained liver dysfunction after prior anesthetic exposure, hypovolemic patients, and those with severe left ventricular dysfunction or pheochromocytoma.

55
Q

What drugs exacerbate myocardial depression with halothane?

A

Beta-adrenergic-blocking agents and calcium channel blockers.

56
Q

What is a serious drug interaction involving halothane and aminophylline?

A

The combination of halothane and aminophylline can cause serious ventricular arrhythmias.

57
Q

What are the physical properties of isoflurane?

A

Isoflurane is a nonflammable volatile anesthetic with a pungent ethereal odor and distinct physicochemical properties.

58
Q

How does isoflurane affect the cardiovascular system?

A

Isoflurane causes minimal left ventricular depression, decreases systemic vascular resistance, and lowers arterial blood pressure while maintaining cardiac output by increasing heart rate.

59
Q

What are the respiratory effects of isoflurane?

A

Isoflurane causes respiratory depression with less tachypnea, leading to a pronounced fall in minute ventilation and blunts ventilatory response to hypoxia and hypercapnia.

60
Q

How does isoflurane affect the cerebral system?

A

Isoflurane increases CBF and intracranial pressure at >1 MAC, but these effects are less pronounced than halothane and can be reversed by hyperventilation.

61
Q

At what concentration does isoflurane produce an electrically silent EEG?

A

At 2 MAC.

62
Q

How does isoflurane affect renal function?

A

It decreases renal blood flow, glomerular filtration rate, and urinary output.

63
Q

How does isoflurane affect hepatic function?

A

Total hepatic blood flow is reduced, but hepatic oxygen supply is better maintained than with halothane.

64
Q

What are the biotransformation products of isoflurane?

A

Isoflurane is metabolized to trifluoroacetic acid, but nephrotoxicity and significant hepatic dysfunction are extremely rare.

65
Q

What are contraindications for isoflurane?

A

Patients with severe hypovolemia may not tolerate its vasodilating effects, and it can trigger malignant hyperthermia.

66
Q

What drugs interact with isoflurane?

A

Epinephrine can be safely administered up to 4.5 mcg/kg, and isoflurane potentiates nondepolarizing neuromuscular blocking agents.

67
Q

What are the physical properties of desflurane?

A

Desflurane is structurally similar to isoflurane with a fluorine substitution, giving it high vapor pressure, low blood solubility, and ultrashort duration of action.

68
Q

How does desflurane affect the cardiovascular system?

A

It decreases systemic vascular resistance and arterial blood pressure, with minimal effect on cardiac output at 1–2 MAC, but rapid increases in concentration can cause transient tachycardia and hypertension.

69
Q

Why is desflurane not ideal for inhalation induction?

A

Its pungency can cause airway irritation, coughing, salivation, and laryngospasm.

70
Q

What are the cerebral effects of desflurane?

A

It increases CBF and intracranial pressure, but also decreases CMRO2 and maintains responsiveness to changes in Paco2.

71
Q

How does desflurane affect renal function?

A

It causes no significant nephrotoxic effects, but reductions in cardiac output can decrease urine output and glomerular filtration.

72
Q

What is the primary toxicity concern with desflurane?

A

Desiccated CO2 absorbent can degrade desflurane to carbon monoxide, posing a risk of carbon monoxide poisoning.

73
Q

What are contraindications for desflurane?

A

Severe hypovolemia, malignant hyperthermia, and intracranial hypertension.

74
Q

What are the physical properties of sevoflurane?

A

Sevoflurane is a halogenated volatile anesthetic with low blood solubility, nonpungency, and a modest vapor pressure, making it ideal for inhalation induction.

75
Q

How does sevoflurane affect the cardiovascular system?

A

Sevoflurane mildly depresses myocardial contractility and lowers systemic vascular resistance and arterial blood pressure, with minimal effect on heart rate.

76
Q

What are the respiratory effects of sevoflurane?

A

It depresses respiration and reverses bronchospasm, similar to isoflurane.

77
Q

How does sevoflurane affect cerebral blood flow?

A

Sevoflurane slightly increases CBF and intracranial pressure, but autoregulation is generally maintained better than with isoflurane.

78
Q

What is the primary concern with sevoflurane metabolism?

A

Sevoflurane can be degraded to compound A by CO2 absorbents, but this rarely causes nephrotoxicity in clinical practice.

79
Q

What precautions are recommended with sevoflurane?

A

Fresh gas flows should be at least 2 L/min for prolonged anesthesia to minimize compound A accumulation.

80
Q

What are contraindications for sevoflurane?

A

Severe hypovolemia, susceptibility to malignant hyperthermia, and intracranial hypertension.

81
Q

What is the anesthetic mechanism of xenon?

A

Xenon inhibits NMDA receptors by competing with glycine at its binding site.

82
Q

What are the advantages of xenon as an anesthetic?

A

Xenon has minimal effects on cardiovascular, hepatic, and renal systems, and provides protection against neuronal ischemia.

83
Q

Why is xenon not widely used?

A

High cost and limited availability due to its complex distillation process.

AAA-ANESTHESIOLOGY (9 decks)

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