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