3. Old stuff
          3.1. Old pharm stuff (pre 2009)
              3.1.3. Pharmacology
                  3.1.3.2. Inhalational anaesthetic agents
                      3.1.3.2.5. Comparisons of inhalational agents
 3.1.3.2.5.3. Respiratory effects of inhalational anaesthetic agents 

Respiratory effects of AA

[SH4:p60]

AA produce dose-dependent effects on

  1. Breathing pattern
  2. Ventilatory response to PaCO2
  3. Ventilatory response to PaO2
  4. Airway resistance

1. Breathing pattern

All AA:

  • Increased RR
    * Due to CNS stimulation
  • Decreased tidal volume
  • Overall decrease in minute volume
    --> Increase in PaCO2

Comparison between AAs

Under 1 MAC

  • All AA produce similar changes in breathing patterns

Over 1 MAC

  • isoflurane does not produce further increase in RR
  • N2O increase RR more than other AAs
    * May also stimulate pulmonary stretch receptors

Awake vs anaesthesia

  • Under anaesthesia, spontaneous breathing is regular and rhythmic
  • When awake, spontaneous breathing has intermittent deep breaths separated by varying intervals

2. Ventilatory response to PaCO2

  • Decreased response to PaCO2
    * CO2 response curve is decreased and shifted right
  • Increased PaCO2
  • Apneic threshold (maximal PaCO2 which does not initiate spontaneous breathing)
    --> Only 3 to 5mmHg lower than PaCO2 during spontaneous breathing

Comparison between AAs

  • Desflurane and sevoflurane produced profound decrease in ventilation
    --> Apnoea between 1.5 to 2 MAC
  • N2O does not increase PaCO2
    * But still depress response to PaCO2

Factors affecting the increase in PaCO2

  • Concurrent use of N2O
    --> PaCO2 increase not as high
  • Surgical stimulation
    * Minute volume increase by 40% due to increased tidal volume and RR
    * CO2 production increase due to sympathetic stimulation
    * Overall PaCO2 drops by 10% (compared to the raised level)
  • Duration of anaesthesia
    * After 5 hours, slope and position of CO2 response curve returns towards normal
  • COPD
    * Accentuate the increase in PaCO2

Mechanism of depression

Mostly due to
* Direct depressant effect on medullary ventilatory centre

  • For halothane (and maybe AA)
    --> Also some action on intercostal muscles
    --> Loss of chest wall stabilisation
    --> Less chest expansion, possibly even chest wall collapse during diaphragmatic inspiration
  • For sevoflurane
    --> Also depression of diaphragmatic contractility

3. Ventilatory response to PaO2

  • All AA profoundly depress ventilatory response to hypoxemia
  • Synergistic effect of low PaO2 and high PaCO2 are lost
  • At 0.1 MAC
    --> 50-70% depression
  • At 1.1 MAC
    --> 100% depression

Sevoflurane vs morphine

  • Depressant effect of sevoflurane on hypoxemia response is equal for both gender
  • Depressant effect of morphine on hypoxemia response is greater in women

4. Airway resistance

Risk factors for bronchospasm during anaesthesia

  • Young age (<10 yo)
  • Perioperative respiratory infection
  • Endotracheal intubation
  • COPD

Comparison between AAs

  • Isoflurane and sevoflurane produce bronchodilation in COPD patients
  • Desflurane is likely to produce bronchoconstriction in smoker
  • Sevoflurane and desflurane might not produce bronchospasm in asthmatic

Sevoflurane

Sevoflurane can react with desiccated CO2 absorbers, especially those with KOH
--> Possible production of toxic gas and irritant

  • Compound A is NOT an airway irritant
  • Formaldehyde is an airway irritant

Functional residual capacity (FRC)

  • N2O and other AAs decrease FRC
    --> May be worsened by N2O-induced skeletal muscle rigidity