Respiratory effects of AA

[Ref: 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 breathng patterns

Over 1 MAC

• ISO 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

• DES and SEV 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 HAL (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 SEV
  --> 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

SEVO vs morphine

Depressant effect of SEVO 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

ISO and SEVO produce bronchodilation in COPD patietns

DES is likely to produce bronchoconstriction in smoker

SEVO and DES might not produce bronchospasm in asthmatic

SEVO

SEVO 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