• Neurocirculatory Responses:  Desflurane (Suprane)

  • Management of rapid increases in BP/heart rate resulting from changes in surgical stimulation intensity --

    • Desflurane (Suprane) effective due to solubility properties

  • Rapid changes in alveolar desflurane (Suprane;e.g., 4% to 12%) (or isoflurane (Forane)) concentrations induce increased sympathetic and renin-angiotensin system activity, increasing heart rate and arterial pressure

  • Sites mediating effect are localized in the upper airway and lungs

    • Not observed with sevoflurane (Sevorane, Ultane)

  • Reduction in cardiovascular responses to rapid changes in desflurane (Suprane) concentration:

    • Pre-treatment

      •  Fentanyl (Sublimaze) (IV five minutes before abrupt desflurane (Suprane) concentration increase)

      •  Esmolol (Brevibloc) (IV 1.5 minutes before desflurane (Suprane) concentration increased)

      •  Clonidine (Catapres) (PO 90 minutes before)

      •  Fentanyl (Sublimaze) pre-treatment -- most clinically useful because

        • Minimal cardiovascular depressive action

        • Little post-anesthetic sedation

• Preexisting myocardial disease and inhaled anesthetic effects

  • Enhanced myocardial depression in patients with pre-existing impaired contractility

  • Myocardial depression following 40% nitrous oxide administration, occurs in patients with coronary vascular disease (not observed in patients without heart disease)

  • Anesthetic-induced circulatory effects and valvular heart disease

    • Isoflurane (Forane)-mediated peripheral vasodilation: undesirable in patients with aortic stenosis

    • Isoflurane (Forane)-mediated peripheral vasodilation: possibly beneficial in patients with mitral or aortic regurgitation

  • Arterial hypoxemia: enhancement of volatile anesthetic-mediated cardiac depression

  • Prior drug therapy -- sympathetic nervous system

    • Magnitude of  volatile agents effects influenced by the presence of  antihypertensive agents and beta-adrenergic blocking drugs

• Ventilation Effects due to inhaled anesthetics: changes in breathing pattern, ventilatory response to CO₂, ventilatory response to arterial hypoxemia and airway resistance

  • Breathing Pattern Effects:

    •  Dose-dependent increases in breathing frequency

      • Isoflurane (Forane) increases breathing frequency in a manner comparable to other agents up to a dose of 1 MAC (> 1 MAC, no further increase)

      • Nitrous oxide increases frequency to a greater extent than other agents at concentrations > 1 MAC

      • Mechanism: CNS stimulation

    • Reduced tidal volume associated with increases in breathing frequency

    • Decreases in tidal volume, despite increases in breathing frequency, causes a decrease in minute ventilation and an increase in PaCO₂.

    •  Breathing pattern under anesthesia: regular and rhythmic (awake pattern: intermittent deep breaths separated by varying intervals of time(

• Ventilatory Response to CO₂

  • Volatile anesthetics:

    •  Dose-dependent ventilation depression

    •  Reduction in ventilatory response to CO₂ and increases in PaCO₂

  • Desflurane (Suprane) and sevoflurane (Sevorane, Ultane): causes apnea between 1.5-2 MAC

    •  Increase PaCO₂

    •  Decrease ventilatory response to CO₂

  •  COPD patients: increased volatile anesthetic-mediated PaCO₂ elevation

  • Nitrous oxide does not increase PaCO₂ (nitrous oxide use may permit reduction of volatile anesthetic causing less ventilation depression)

    •  Ventilation-depressants-sparing nitrous oxide effect: observed with all volatile anesthetics

• Surgical Stimulation

  • Increases minute ventilation by about 40%, secondary to increasing tidal volume and breathing frequency.

  • PaCO₂ decreases about 10%, despite increased minute ventilation -- mechanism: probably enhanced sympathetic nervous system activity caused by surgical stimulation.

    •  Increased sympathetic activity causes increased CO₂ production

• Mechanism of Anesthetic-induced ventilation depression

  •  Depression of medullary ventilatory center

  •  Possible reduction in intercostal muscle function, interfering with normal chest expansion

    •  This loss of chest wall stabilization interferes with normal diaphragmatic function

• Ventilatory depression (volatile anesthetics): Management

  • Mechanical ventilation

• Hypoxemia: Ventilatory response

  • Inhaled anesthetics: depress ventilatory response to hypoxemia ( response normally carotid body-mediated)

    •  0.1 MAC: 50%-70% depression

    •  1.1 MAC: 100% depression

• Airway Resistance (volatile anesthetics)

  • Dose-dependent reduction in airway resistance is typically observed in the presence of underlying above-average bronchomotor tone (bronchoconstriction)

  • Halothane (Fluothane)-- reduction in airway resistance due to:

    •   Diminished vagal effect on airway smooth muscle

  • Sevoflurane (Sevorane, Ultane) and desflurane (Suprane): no evidence of promoting bronchospasm in patients with asthma

  • Halothane (Fluothane) and enflurane (Ethrane): reverse bronchoconstrictive effects of hypocapnia

    •  Prevents/reverses bronchoconstriction in patients with asthma

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