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 & renin-angiotensin system activity, increasing heart rate & arterial pressure

• Sites mediating effect are localized in the upper airway & 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 & 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 & 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 & beta-adrenergic blocking drugs

Ventilation Effects due to inhaled anesthetics: changes in --breathing pattern, ventilatory response to CO₂, ventilatory response to arterial hypoxemia & 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 & 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) & 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 & 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-- 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) & desflurane (Suprane): no evidence of promoting bronchospasm in patients with asthma

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

  •  Prevents/reverses bronchoconstriction in patients with asthma