INHALATIONAL ANESTHESIA Flashcards
What is general anesthesia characterized by?
Reversible loss of consciousness, analgesia, amnesia, and some degree of muscle relaxation.
Which substances are capable of producing general anesthesia?
Inert elements (xenon), simple inorganic compounds (nitrous oxide), halogenated hydrocarbons (halothane), ethers (isoflurane, sevoflurane, desflurane), and complex organic structures (propofol).
What receptors do nitrous oxide and xenon inhibit?
N-methyl-D-aspartate (NMDA) receptors.
What effects are mediated by gamma-aminobutyric acid (GABA) receptors in anesthesia?
Anesthetic effects through enhanced chloride channel conductance and inhibition in the CNS.
Which brain areas are affected by anesthetics?
Reticular activating system, cerebral cortex, cuneate nucleus, olfactory cortex, hippocampus, and the spinal cord.
What is the significance of cortical and subcortical anesthetic action?
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.
Where does MAC measurement suggest anesthetic effects occur?
Primarily at the spinal cord rather than the cerebral cortex.
What is the Meyer–Overton rule?
Anesthetic potency of inhalation agents correlates with their lipid solubility.
What does the critical volume hypothesis propose?
Anesthetics expand the lipid bilayer of membranes, altering their function.
What reverses anesthesia as proposed by the critical volume hypothesis?
Increased hydrostatic pressure.
How do inhalational agents modulate GABA receptors?
By binding to hydrophobic domains in GABA channel proteins, enhancing their inhibitory activity.
What other ion channels may play a role in anesthetic action?
Glycine receptors, nicotinic acetylcholine receptors, and NMDA receptors.
What concern is raised about general anesthetics in children?
Early exposure may promote cognitive impairment or neuronal apoptosis.
Which inhalational agent is linked to apoptosis in animal studies?
Isoflurane.
What is the role of xenon in neuroprotection?
It inhibits calcium influx after cell injury, reducing apoptosis.
What is the minimum alveolar concentration (MAC)?
The alveolar concentration that prevents movement in 50% of patients in response to a stimulus.
How does MAC relate to potency comparisons between anesthetic agents?
It mirrors brain partial pressure, allowing standardized potency comparisons.
How do MAC values of different anesthetics interact?
MAC values are roughly additive, e.g., 0.5 MAC nitrous oxide + 0.5 MAC halothane = 1.0 MAC.
How is MAC altered with aging?
MAC decreases by about 6% per decade of age.
What does 1.3 MAC represent clinically?
It prevents movement in approximately 95% of patients (similar to ED95).
What factors do not affect MAC?
Species, sex, and duration of anesthesia.
Where is the hypothesized site of motor inhibition by anesthetics?
The spinal cord, as MAC is unaffected by spinal cord transection in rats.
What is ischemic preconditioning?
A brief ischemic event protects cells from future ischemic injury.
What cardiac channel is involved in anesthetic preconditioning?
ATP-sensitive potassium (KATP) channels.
Which markers indicate myocardial protection by sevoflurane?
Reduced levels of troponin T.
Which volatile anesthetics have been linked to both neurotoxicity and neuroprotection?
Isoflurane and sevoflurane.
How does reactive oxygen species (ROS) relate to anesthetic injury?
ROS are associated with cellular damage, which anesthetics like xenon may reduce by inhibiting calcium influx.
How is MAC useful for experimental evaluations?
It provides a standard for comparing anesthetic effects and potencies.
At what MAC is awakening from anesthesia likely to occur?
0.3–0.4 MAC for most inhaled agents.
What are the physical properties of nitrous oxide?
Nitrous oxide is colorless, essentially odorless, nonflammable, and stored as a liquid under pressure because its critical temperature is above room temperature.
What receptor does nitrous oxide antagonize?
N-methyl-D-aspartate (NMDA) receptor.
How does nitrous oxide affect the cardiovascular system?
It stimulates the sympathetic nervous system, slightly increasing blood pressure, cardiac output, and heart rate in vivo, despite direct myocardial depression in vitro.
What is the effect of nitrous oxide on pulmonary vascular resistance?
Nitrous oxide increases pulmonary vascular resistance and modestly elevates right ventricular end-diastolic pressure.
How does nitrous oxide affect respiratory function?
It increases respiratory rate (tachypnea) and decreases tidal volume, with minimal change in minute ventilation and arterial CO2 levels.
Why is hypoxic drive a concern with nitrous oxide use?
Nitrous oxide markedly depresses hypoxic drive, even at small concentrations.
What are the cerebral effects of nitrous oxide?
It increases cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and intracranial pressure.
Does nitrous oxide provide muscle relaxation?
No, nitrous oxide does not provide significant muscle relaxation and may cause skeletal muscle rigidity at high concentrations.
How does nitrous oxide affect renal function?
Nitrous oxide decreases renal blood flow, glomerular filtration rate, and urinary output.
What is the primary route of nitrous oxide elimination?
Almost all nitrous oxide is eliminated via exhalation.
What is a potential toxicity of nitrous oxide related to vitamin B12?
Nitrous oxide irreversibly oxidizes the cobalt atom in vitamin B12, inhibiting methionine synthetase and thymidylate synthetase, potentially causing megaloblastic anemia and peripheral neuropathy.
Why is nitrous oxide often avoided in early pregnancy?
Nitrous oxide may have teratogenic effects and is avoided in pregnant patients not in the third trimester.
What is a contraindication for nitrous oxide related to air-containing cavities?
Nitrous oxide rapidly diffuses into air-containing cavities, such as pneumothorax or intracranial air, causing expansion and increased pressure.
What is a significant drug interaction of nitrous oxide with volatile agents?
Nitrous oxide decreases the MAC of volatile agents by approximately 50%.
What is a major environmental concern with nitrous oxide?
Nitrous oxide is an ozone-depleting gas with greenhouse effects.
What are the physical properties of halothane?
Halothane is a halogenated alkane, nonflammable, and stabilized with thymol preservative in amber-colored bottles.
How does halothane affect the cardiovascular system?
Halothane reduces arterial blood pressure and cardiac output dose-dependently and sensitizes the heart to arrhythmogenic effects of epinephrine.
What are the respiratory effects of halothane?
Halothane causes rapid, shallow breathing, decreases tidal volume, and elevates resting PaCO2 levels. It also acts as a potent bronchodilator.
How does halothane affect cerebral blood flow and intracranial pressure?
Halothane dilates cerebral vessels, increasing cerebral blood flow and intracranial pressure, though hyperventilation can prevent these rises.
Is halothane a triggering agent for malignant hyperthermia?
Yes, halothane can trigger malignant hyperthermia.
How does halothane affect renal function?
Halothane reduces renal blood flow, glomerular filtration rate, and urinary output.
What are the hepatic effects of halothane?
Halothane decreases hepatic blood flow and can impair drug metabolism and clearance. It is also associated with rare cases of halothane hepatitis.
What is the mechanism of halothane metabolism?
Halothane is oxidized in the liver to trifluoroacetic acid, with minor reductive metabolites under hypoxic conditions.
What patients are at increased risk for halothane hepatitis?
Middle-aged obese women, those exposed to multiple halothane anesthetics, and individuals with familial predisposition to halothane toxicity.
What are contraindications for halothane use?
Unexplained liver dysfunction after prior anesthetic exposure, hypovolemic patients, and those with severe left ventricular dysfunction or pheochromocytoma.
What drugs exacerbate myocardial depression with halothane?
Beta-adrenergic-blocking agents and calcium channel blockers.
What is a serious drug interaction involving halothane and aminophylline?
The combination of halothane and aminophylline can cause serious ventricular arrhythmias.
What are the physical properties of isoflurane?
Isoflurane is a nonflammable volatile anesthetic with a pungent ethereal odor and distinct physicochemical properties.
How does isoflurane affect the cardiovascular system?
Isoflurane causes minimal left ventricular depression, decreases systemic vascular resistance, and lowers arterial blood pressure while maintaining cardiac output by increasing heart rate.
What are the respiratory effects of isoflurane?
Isoflurane causes respiratory depression with less tachypnea, leading to a pronounced fall in minute ventilation and blunts ventilatory response to hypoxia and hypercapnia.
How does isoflurane affect the cerebral system?
Isoflurane increases CBF and intracranial pressure at >1 MAC, but these effects are less pronounced than halothane and can be reversed by hyperventilation.
At what concentration does isoflurane produce an electrically silent EEG?
At 2 MAC.
How does isoflurane affect renal function?
It decreases renal blood flow, glomerular filtration rate, and urinary output.
How does isoflurane affect hepatic function?
Total hepatic blood flow is reduced, but hepatic oxygen supply is better maintained than with halothane.
What are the biotransformation products of isoflurane?
Isoflurane is metabolized to trifluoroacetic acid, but nephrotoxicity and significant hepatic dysfunction are extremely rare.
What are contraindications for isoflurane?
Patients with severe hypovolemia may not tolerate its vasodilating effects, and it can trigger malignant hyperthermia.
What drugs interact with isoflurane?
Epinephrine can be safely administered up to 4.5 mcg/kg, and isoflurane potentiates nondepolarizing neuromuscular blocking agents.
What are the physical properties of desflurane?
Desflurane is structurally similar to isoflurane with a fluorine substitution, giving it high vapor pressure, low blood solubility, and ultrashort duration of action.
How does desflurane affect the cardiovascular system?
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.
Why is desflurane not ideal for inhalation induction?
Its pungency can cause airway irritation, coughing, salivation, and laryngospasm.
What are the cerebral effects of desflurane?
It increases CBF and intracranial pressure, but also decreases CMRO2 and maintains responsiveness to changes in Paco2.
How does desflurane affect renal function?
It causes no significant nephrotoxic effects, but reductions in cardiac output can decrease urine output and glomerular filtration.
What is the primary toxicity concern with desflurane?
Desiccated CO2 absorbent can degrade desflurane to carbon monoxide, posing a risk of carbon monoxide poisoning.
What are contraindications for desflurane?
Severe hypovolemia, malignant hyperthermia, and intracranial hypertension.
What are the physical properties of sevoflurane?
Sevoflurane is a halogenated volatile anesthetic with low blood solubility, nonpungency, and a modest vapor pressure, making it ideal for inhalation induction.
How does sevoflurane affect the cardiovascular system?
Sevoflurane mildly depresses myocardial contractility and lowers systemic vascular resistance and arterial blood pressure, with minimal effect on heart rate.
What are the respiratory effects of sevoflurane?
It depresses respiration and reverses bronchospasm, similar to isoflurane.
How does sevoflurane affect cerebral blood flow?
Sevoflurane slightly increases CBF and intracranial pressure, but autoregulation is generally maintained better than with isoflurane.
What is the primary concern with sevoflurane metabolism?
Sevoflurane can be degraded to compound A by CO2 absorbents, but this rarely causes nephrotoxicity in clinical practice.
What precautions are recommended with sevoflurane?
Fresh gas flows should be at least 2 L/min for prolonged anesthesia to minimize compound A accumulation.
What are contraindications for sevoflurane?
Severe hypovolemia, susceptibility to malignant hyperthermia, and intracranial hypertension.
What is the anesthetic mechanism of xenon?
Xenon inhibits NMDA receptors by competing with glycine at its binding site.
What are the advantages of xenon as an anesthetic?
Xenon has minimal effects on cardiovascular, hepatic, and renal systems, and provides protection against neuronal ischemia.
Why is xenon not widely used?
High cost and limited availability due to its complex distillation process.
