Exam 3 Inhalation Agents
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Questions and Answers

The potency of anesthetic agents is measured by:

  • Alveolar partial pressure
  • MAC immobility (correct)
  • MAC amnesia
  • $EC_{50}$
  • Which of the following determines the input (delivery) of an inhaled anesthetic into the alveoli?

  • Blood gas coefficient and MAC
  • Cardiac output and alveolar-to-venous partial pressure difference
  • Alveolar ventilation and solubility
  • PI (partial pressure), alveolar ventilation, and uptake of the breathing system (correct)
  • The second gas effect is characterized by:

  • The ability of a gas to slow down the uptake of other gases
  • The ability of a gas to induce anesthesia
  • The ability of a gas to decrease the concentration of other gases in the alveoli
  • The ability of a gas to increase the concentration of other gases in the alveoli (correct)
  • What is the mechanism by which immobility is mediated at the spinal cord?

    <p>Depressing AMPA and NMDA currents</p> Signup and view all the answers

    What is the relationship between MAC amnesia, MAC unconsciousness, and MAC immobility?

    <p>MAC amnesia is lower than MAC unconsciousness which is lower than MAC immobility</p> Signup and view all the answers

    When nitrous oxide is used as a carrier gas, what effect does it have on inhalational anesthetic agents?

    <p>It speeds up the onset of inhalational anesthetic agents due to the second gas effect</p> Signup and view all the answers

    What is the purpose of controlling the inspired partial pressure of an inhaled anesthetic?

    <p>To achieve a constant and optimal brain partial pressure of the anesthetic</p> Signup and view all the answers

    What occurs when nitrous oxide is discontinued abruptly?

    <p>A reversal of partial pressure gradients such that nitrous oxide leaves the blood to enter the alveoli</p> Signup and view all the answers

    Other than the lungs, what is the primary organ responsible for the metabolism of halothane?

    <p>Liver</p> Signup and view all the answers

    What is the primary route of elimination for inhaled anesthetics?

    <p>Lungs</p> Signup and view all the answers

    What determines the metabolism of inhaled anesthetics?

    <p>All of the above</p> Signup and view all the answers

    What is the purpose of the absorption phase in inhaled anesthesia?

    <p>To deliver the anesthetic from the anesthetic machine to alveoli to the pulmonary capillary blood</p> Signup and view all the answers

    What is the effect of halothane on cardiac output and inotropy?

    <p>Decreases cardiac output and inotropy</p> Signup and view all the answers

    What is the effect of sevoflurane on bronchiole smooth muscle tone/airways resistance?

    <p>Produces bronchodilation</p> Signup and view all the answers

    What is the effect of age on MAC?

    <p>MAC decreases with age</p> Signup and view all the answers

    What is the effect of opioids on inhaled anesthetic requirements?

    <p>Decreases inhaled anesthetic requirements</p> Signup and view all the answers

    What is the effect of N2O on pulmonary vascular resistance?

    <p>Increases pulmonary vascular resistance</p> Signup and view all the answers

    What is the effect of inhalation agents on renal blood flow and GFR?

    <p>Decreases renal blood flow and GFR in a dose-dependent fashion.</p> Signup and view all the answers

    What is the effect of halothane on cardiac dysrhythmia?

    <p>Increases the risk of cardiac dysrhythmia</p> Signup and view all the answers

    What is the effect of isoflurane, desflurane, and sevoflurane on systemic vascular resistance?

    <p>Decreases systemic vascular resistance due to decreased SVR</p> Signup and view all the answers

    What is the effect of inhaled anesthetics on cerebral blood flow?

    <p>Increases cerebral blood flow</p> Signup and view all the answers

    What is the primary mechanism by which inhaled anesthetics exert their effects on inhibitory glycine receptors, leading to a decrease in neuronal activity?

    <p>Potentiation</p> Signup and view all the answers

    What is the primary factor that determines the metabolism of inhaled anesthetics?

    <p>All of the above</p> Signup and view all the answers

    What is the primary site of elimination for inhaled anesthetics?

    <p>Lungs</p> Signup and view all the answers

    Which of the following inhalation agents is most likely to increase sympathetic tone and also PVR?

    <p>Nitrous oxide</p> Signup and view all the answers

    What is the effect of halothane on hepatic function?

    <p>All of the above</p> Signup and view all the answers

    What is the effect of inhaled anesthetics on ventilation?

    <p>Increase the rate and decrease depth of ventilation</p> Signup and view all the answers

    A patient is receiving an inhalation anesthetic and has a history of cardiac disease. What is the most likely complication?

    <p>Myocardial depression</p> Signup and view all the answers

    What is the relationship between the partial pressure of the inhaled anesthetic (PI) and the partial pressure of the anesthetic in the arterial blood (PA) according to the concentration effect?

    <p>The higher the PI, the more rapidly PA approaches PI</p> Signup and view all the answers

    What is the result of the a higher concentration of anesthetic on induction of anesthesia?

    <p>Faster onset of anesthesia</p> Signup and view all the answers

    What are potential complications related to the usage of inhaled nitrous oxide?

    <p>All of the above</p> Signup and view all the answers

    Which anesthetic is metabolized in the liver the most?

    <p>Halothane (15-20%)</p> Signup and view all the answers

    Which of the following anesthetics undergoes more extensive intrarenal metabolism than sevoflurane?

    <p>Enflurane</p> Signup and view all the answers

    What is the result of desflurane exposure to dry CO2 absorbent?

    <p>Production of carbon monoxide (CO)</p> Signup and view all the answers

    What is the result of sevoflurane exposure to dry CO2 absorbent?

    <p>Production of compound A, which is nephrotoxic</p> Signup and view all the answers

    What factors decrease Compound A generation?

    <p>Higher fresh gas flow and lower absorbent temperature</p> Signup and view all the answers

    What is MAC (Minimum Alveolar Concentration) defined as in terms of skeletal muscle movement?

    <p>The concentration at 1 atmosphere preventing skeletal muscle movement in response to supramaximal painful stimulation in 50% of patients</p> Signup and view all the answers

    What changes in the elderly population can make anesthetics more potent at smaller volumes?

    <p>Decreases in lean body mass, increases in fat, and decreased cardiac output</p> Signup and view all the answers

    What is the result of a heart being exposed to another ischemic event after brief ischemic preconditioning?

    <p>Reduced sensitivity to ischemic or hypoxic insult</p> Signup and view all the answers

    What is the common mechanism by which myocardial ischemic preconditioning and volatile inhalation agents protect the heart?

    <p>Hyperpolarization of potassium channels, leading to decreased sensitivity to subsequent ischemia</p> Signup and view all the answers

    Which type of muscle receptors do volatile agents inhibit, and what effect do they have on neuromuscular blocking drugs?

    <p>nicotinic receptors, potentiate</p> Signup and view all the answers

    All volatile agents can trigger MH with halothane being the most potent trigger

    <p>True</p> Signup and view all the answers

    All volatile agents have little to no effect on PVR

    <p>True</p> Signup and view all the answers

    Volatile anesthetics increase renal blood flow and GFR in a dose-dependent fashion

    <p>False</p> Signup and view all the answers

    What impact does preoperative hydration have on reduced renal blood flow related to volatile anesthetic administration?

    <p>It attenuates the reduction in renal blood flow.</p> Signup and view all the answers

    How does hyperventilation to a PaCO2 of 30 affect the intracranial pressure (ICP) during inhalation anesthetic administration?

    <p>It decreases ICP</p> Signup and view all the answers

    What is the relationship between MAC (minimum alveolar concentration) and potency in anesthetics?

    <p>A lower MAC indicates a more potent anesthetic</p> Signup and view all the answers

    What are risk factors for bronchospasm secondary to inhalation agents?

    <p>All of the above</p> Signup and view all the answers

    What is the effect of inhaled anesthetics on ventilation and the ventilatory response to hypoxemia?

    <p>They blunt the ventilatory response to hypoxemia with 100% depression at 1.1 MAC</p> Signup and view all the answers

    Unlike other inhaled anesthetics, nitrous oxide preserves tidal volume

    <p>True</p> Signup and view all the answers

    How do inhalation anesthetics work?

    <p>All of the above</p> Signup and view all the answers

    What are complications associated with enflurane use? (select 2)

    <p>Lowered seizure threshold</p> Signup and view all the answers

    Which inhaled anesthetic has a higher risk of bronchospasm due to its pungent odor?

    <p>Desflurane</p> Signup and view all the answers

    Which of the following inhaled anesthetics are associated with causing tachycardia? (select 3)

    <p>Desflurane</p> Signup and view all the answers

    Why does halothane potentiate cardiac arrhythmias and bradycardia?

    <p>All of the above</p> Signup and view all the answers

    What impact does a higher blood:gas coefficient have on the rate of induction?

    <p>Slower induction</p> Signup and view all the answers

    What is the relationship between the rate of rise of PA (arterial pressure) and the solubility of the inhalation agent in blood?

    <p>Inversely proportional</p> Signup and view all the answers

    How does anemia affect the blood:gas coefficient (BGC) and equilibration?

    <p>It decreases the BGC and hastens equilibration.</p> Signup and view all the answers

    What factors does tissue uptake of inhalation agents depend on?

    <p>Solubility, blood flow, and arterial to tissue pressure differences</p> Signup and view all the answers

    Where does the inhalation agent primarily move from during the elimination phase?

    <p>Blood to alveoli</p> Signup and view all the answers

    What determines continued uptake or removal in other tissues of inhaled anesthetics (context sensitive half time)?

    <p>Solubility and duration of exposure</p> Signup and view all the answers

    Why should the washout of inhaled anesthetics from the brain be rapid?

    <p>Inhaled anesthetics are not highly soluble in brain</p> Signup and view all the answers

    Is it true that all volatile anesthetic agents increase cutaneous blood flow, potentiating heat loss during anesthesia?

    <p>True</p> Signup and view all the answers

    What is the effect of halothane, isoflurane, and desflurane on CVP?

    <p>It will increase</p> Signup and view all the answers

    Which inhaled anesthetic may provoke nausea and vomiting?

    <p>Nitrous oxide</p> Signup and view all the answers

    Which 2 inhaled anesthetic produces the most pronounced effect of beta-2 receptor stimulation, resulting in mild bronchodilation at higher concentrations?

    <p>Sevoflurane</p> Signup and view all the answers

    What effect does the increased respiratory rate and decreased tidal volume in inhalation agents have on PaCO2 levels and alveolar ventilation?

    <p>PaCO2 levels increase and alveolar ventilation decreases - due to increased dead space ventilation</p> Signup and view all the answers

    At MAC < 0.4, what happens to EEG frequency and voltage?

    <p>EEG frequency and voltage increase (Excitement/Stage 2)</p> Signup and view all the answers

    What type of receptors are AMPA and NMDA receptors?

    <p>Glutamate (excitatory) receptors</p> Signup and view all the answers

    Increased HR and BP is most likely to occur with abrupt increases in which anesthetic?

    <p>Desflurane</p> Signup and view all the answers

    Which of the following is increased by hyperthermia?

    <p>MAC (minimum alveolar concentration)</p> Signup and view all the answers

    Nitrous oxide is most capable of supporting combustion

    <p>True</p> Signup and view all the answers

    What MAC (Minimum Alveolar Concentration) prevents movement in response to surgical stimulus in 95% of patients?

    <p>1.3</p> Signup and view all the answers

    What is the mechanism by which inhalation agents cause a rise in PaCO2 and decreased alveolar ventilation?

    <p>Increased dead space ventilation (increased RR) and ineffective CO2 elimination (decreased tidal volume)</p> Signup and view all the answers

    Based on the ASA Statement in 2023, what is the normal fresh gas flow (FGF) rate that most adults can be managed with?

    <p>0.5 L/min</p> Signup and view all the answers

    Study Notes

    Volatile Inhalation Agents and N2O

    • Relative potency (MAC) of an anesthetic agent is measured by immobility, which is mediated by depressing AMPA and NMDA currents in the spinal cord.
    • MAC amnesia is lower than MAC unconsciousness, which is lower than MAC immobility.
    • Blood gas coefficient (BGC) affects the onset and emergence of an anesthetic; a lower BGC results in faster onset and emergence.

    Determinants of Alveolar Partial Pressures

    • PA (arterial pressure) and Pbr (partial pressure in brain) are determined by input (delivery) into the alveoli minus uptake (loss) of the drug from the alveoli into the pulmonary arterial blood.
    • Input depends on PI, alveolar ventilation, and characteristics of the anesthetic breathing system.
    • Uptake depends on solubility, cardiac output (CO), and alveolar-to-venous partial pressure difference (PA - Pv).

    Second Gas Effect

    • High-volume uptake of one gas (first gas) increases the concentration of other gases (second gas) in the alveoli, speeding up the uptake of the second gas.
    • Nitrous oxide (N2O) can speed up the onset of inhalational anesthetic agents when used as a carrier gas.

    Mechanism of Action

    • Inhalation agents may influence K+ channels, protein binding, dissolvability in lipids (Meyer-Overton hypothesis), potentiate inhibitory glycine receptors, decrease neurotransmission at glutamate receptors, and block the effects of NMDA receptors.

    Administration and Induction

    • The primary objective of inhaled anesthesia is to achieve a constant and optimal brain partial pressure (Pbr) of the anesthetic.
    • Factors influencing the rate of anesthetic induction include age, co-existing disease, and co-administration of other pharmacologic agents.
    • Low cardiac output can lead to abrupt increases in alveolar pressure.

    Metabolism and Elimination

    • Absorption/Solubility: from vaporizer to alveoli to pulmonary capillary.
    • Distribution: from capillary to site of action.
    • Metabolism: liver or renal, depending on the agent's chemical structure, hepatic enzyme activity, genetic factors, and blood concentration.
    • Elimination/Recovery: primarily through the lungs, with continued uptake/removal in other tissues depending on solubility and duration of exposure.

    Factors Influencing MAC

    • MAC is inversely affected by age.
    • Decreased during pregnancy and returns to baseline in 12-72 hours.
    • Red hair coupled with female gender increases MAC.
    • MAC values for inhaled agents are additive.
    • Opioids synergistically reduce inhaled anesthetic requirements.

    Complications

    • Cardiac dysrhythmia: halothane has a risk of cardiac depression and ventricular tachycardia (VT).
    • Hepatic disease: halothane has a risk of postoperative hepatic dysfunction.
    • Kidney injury: enflurane and sevoflurane can cause kidney damage due to nephrotoxic compounds produced during metabolism.
    • Hypotension: decreases in MAP are due to decreases in SVR with isoflurane, desflurane, and sevoflurane.

    Influence on Organ Systems

    • Cardiovascular performance:
      • Cardiac output: halothane decreases CO, while isoflurane, desflurane, and sevoflurane increase HR.
      • Systemic vascular resistance: isoflurane, desflurane, and sevoflurane decrease SVR.
    • Respiratory dynamics:
      • Rate and depth of ventilation: inhaled anesthetics increase RR and decrease Vt (except N2O).
      • Bronchiole smooth muscle tone/airways resistance: sevoflurane produces bronchodilation.
    • Renal function: volatile anesthetics decrease renal blood flow and GFR in a dose-dependent fashion.
    • Central nervous system effects:
      • Cerebral blood flow: inhalation agents produce dose-dependent increases in CBF, leading to increases in ICP.
      • EEG: at MAC, EEG changes are observed.

    Volatile Inhalation Agents and N2O

    • Relative potency (MAC) of an anesthetic agent is measured by immobility, which is mediated by depressing AMPA and NMDA currents in the spinal cord.
    • MAC amnesia is lower than MAC unconsciousness, which is lower than MAC immobility.
    • Blood gas coefficient (BGC) affects the onset and emergence of an anesthetic; a lower BGC results in faster onset and emergence.

    Determinants of Alveolar Partial Pressures

    • PA (arterial pressure) and Pbr (partial pressure in brain) are determined by input (delivery) into the alveoli minus uptake (loss) of the drug from the alveoli into the pulmonary arterial blood.
    • Input depends on PI, alveolar ventilation, and characteristics of the anesthetic breathing system.
    • Uptake depends on solubility, cardiac output (CO), and alveolar-to-venous partial pressure difference (PA - Pv).

    Second Gas Effect

    • High-volume uptake of one gas (first gas) increases the concentration of other gases (second gas) in the alveoli, speeding up the uptake of the second gas.
    • Nitrous oxide (N2O) can speed up the onset of inhalational anesthetic agents when used as a carrier gas.

    Mechanism of Action

    • Inhalation agents may influence K+ channels, protein binding, dissolvability in lipids (Meyer-Overton hypothesis), potentiate inhibitory glycine receptors, decrease neurotransmission at glutamate receptors, and block the effects of NMDA receptors.

    Administration and Induction

    • The primary objective of inhaled anesthesia is to achieve a constant and optimal brain partial pressure (Pbr) of the anesthetic.
    • Factors influencing the rate of anesthetic induction include age, co-existing disease, and co-administration of other pharmacologic agents.
    • Low cardiac output can lead to abrupt increases in alveolar pressure.

    Metabolism and Elimination

    • Absorption/Solubility: from vaporizer to alveoli to pulmonary capillary.
    • Distribution: from capillary to site of action.
    • Metabolism: liver or renal, depending on the agent's chemical structure, hepatic enzyme activity, genetic factors, and blood concentration.
    • Elimination/Recovery: primarily through the lungs, with continued uptake/removal in other tissues depending on solubility and duration of exposure.

    Factors Influencing MAC

    • MAC is inversely affected by age.
    • Decreased during pregnancy and returns to baseline in 12-72 hours.
    • Red hair coupled with female gender increases MAC.
    • MAC values for inhaled agents are additive.
    • Opioids synergistically reduce inhaled anesthetic requirements.

    Complications

    • Cardiac dysrhythmia: halothane has a risk of cardiac depression and ventricular tachycardia (VT).
    • Hepatic disease: halothane has a risk of postoperative hepatic dysfunction.
    • Kidney injury: enflurane and sevoflurane can cause kidney damage due to nephrotoxic compounds produced during metabolism.
    • Hypotension: decreases in MAP are due to decreases in SVR with isoflurane, desflurane, and sevoflurane.

    Influence on Organ Systems

    • Cardiovascular performance:
      • Cardiac output: halothane decreases CO, while isoflurane, desflurane, and sevoflurane increase HR.
      • Systemic vascular resistance: isoflurane, desflurane, and sevoflurane decrease SVR.
    • Respiratory dynamics:
      • Rate and depth of ventilation: inhaled anesthetics increase RR and decrease Vt (except N2O).
      • Bronchiole smooth muscle tone/airways resistance: sevoflurane produces bronchodilation.
    • Renal function: volatile anesthetics decrease renal blood flow and GFR in a dose-dependent fashion.
    • Central nervous system effects:
      • Cerebral blood flow: inhalation agents produce dose-dependent increases in CBF, leading to increases in ICP.
      • EEG: at MAC, EEG changes are observed.

    Myocardial Ischemic Preconditioning

    • Myocardial ischemic preconditioning occurs when the myocardium (heart muscle) is briefly exposed to an ischemic event, which triggers a protective mechanism.
    • During this brief ischemic event, potassium channels in the myocardium tend to become hyperpolarized.
    • As a result, when the myocardium is exposed to another ischemic event, the potassium channels do not react, protecting the heart from sustained ischemic or hypoxic insult.
    • Volatile inhalation agents can mimic this protective effect, providing a similar safeguard against ischemic or hypoxic injury when used briefly.

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    Description

    This quiz covers the properties and effects of volatile inhalation anesthetic agents and nitrogen oxide, including their potency, amnesia, and onset/emergence. It also touches on the determinants of alveolar partial pressures.

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