Highlights
- The spinal muscles relax, increasing thoracic spinal curvature; relaxation of intercostal muscles leads to a reduction in the cross-sectional area of the ribcage; and the diaphragm is displaced in a cephalad direction, particularly in dependent regions because of the weight of the abdominal contents. Together, these three changes to the chest cavity shape cause an immediate reduction in functional residual capacity (FRC) of 15–20% compared to the value when awake and supine (View Highlight)
- The reduction in FRC is similar in patients breathing spontaneously and those whose lungs are ventilated artificially, and is much greater in obese patients (View Highlight)
- In older patients, the reduced FRC may be less than the closing capacity and so airway collapse will occur throughout the lung (View Highlight)
- Even if FRC remains above the closing capacity, the changes in chest wall and diaphragm shape commonly result in direct compression of lung tissue in the caudal and dependent regions behind the diaphragm. This leads to atelectasis in 75–90% of patients (View Highlight)
- In an awake subject, both V˙ and Q˙ increase on moving through lung regions from non-dependent areas to dependent areas, with Q˙ increasing slightly more than V˙ (View Highlight)
Fig 1. Electrical impedance tomography of ventilation distribution before and after induction of anaesthesia (white=well ventilated, blue=some ventilation, black=no ventilation). (A) Awake patient showing the normal situation of greater ventilation of the right lung and dependent regions on both sides. (B) Same patient 4 min after GA induction with positive pressure ventilation showing continued greater ventilation of the right lung, but now predominantly non-dependent regional ventilation. The figures show the percentage ventilation to the four quadrants. (View Highlight)- Minute ventilation is significantly reduced during anaesthesia if artificial ventilation is not used: opioids normally slow the ventilatory frequency and inhaled anaesthetics reduce tidal volume, so the usual combination of both drugs causes a profound reduction in ventilation. The normal reflex ventilatory responses to both hypoxia and hypercapnia are also attenuated (View Highlight)
- oxygenation is impaired during GA by four mechanisms: hypercapnia reducing alveolar PO2, abnormal respiratory muscle activity, which leads to shunting of venous blood through areas of atelectasis, and mismatch of ventilation to perfusion leading to areas of lung with low V˙/Q˙ ratios. Abnormal muscle activity and atelectasis cannot be rectified by increasing FIO2, but the other two are easily corrected with quite small increases to around 30–40% inspired oxygen, which normally results in acceptable arterial saturation for most patients. (View Highlight)