Читать книгу Respiratory Medicine - Stephen J. Bourke - Страница 36

To understand this, we first have to remember why we breathe. Whilst oxygen is an essential requirement for life, we do not need the high level of oxygenation usually seen in health for survival. We operate with a substantial margin of safety. This safety margin allows us to vary our ventilation (sometimes at the expense of a normal oxygen level) in order to precisely regulate the CO₂ content of the blood. CO₂ is intimately linked with pH. Whilst it is possible to live for years with lower than normal oxygen levels, we cannot survive long at all with pH outside the normal range. Keeping pH in the normal range is therefore the priority, and CO₂ rather than O₂ is the principal driver of ventilation.

In health, PCO₂ is maintained at very close to 5.3 kPa (40 mmHg). Any increase above this level provokes hyperventilation; any dip leads to hypoventilation. In practice, PCO₂ is so tightly regulated that such fluctuations are not observable. Even when substantial demands are placed on the respiratory system, such as hard physical exercise (with its dramatic increase in O₂ utilisation and CO₂ production), the arterial PCO₂ will barely budge.

Like any finely tuned sensor, however, if the respiratory system is exposed to concentrations it’s not designed to deal with for long periods, it will tend to break. In some patients with chronic lung disease (commonly COPD), the CO₂ sensor begins to fail. Underventilation then occurs, and, over time, PCO₂ drifts upward (and PO₂ downward). Despite the fall in PO₂, initially at least, nothing much happens. Although there is a separate sensor monitoring levels of hypoxia, it remains blissfully unconcerned by modest reductions in PO₂ (because of the margin of safety just discussed). Only when PO₂ reaches a levels that could have an impact on bodily function (around 8 kPa; 60 mmHg) does the hypoxic sensor wake up and decide to take action. Happy to tolerate a certain degree of hypoxia, it won’t allow the PO₂ to fall below this important threshold, which is marginal to the sustainability of life.

When this occurs, hypoxia then takes up the reins as the driver to ventilation and prevents what would have been a progressive decline to death. Once an individual is dependent on this ‘hypoxic drive’, a degree of hypoxia is (obviously) necessary to drive ventilation. This is not always appreciated. At times, a ‘high‐flow’ oxygen mask may be applied to a patient by a well‐meaning doctor in an attempt to raise the PO₂ to a more ‘normal’ level. But no hypoxia means no drive to breathe. The result can be catastrophic underventilation, which, if not dealt with properly, can be fatal. When treating hypoxic patients who may have chronic lung disease, until their ventilatory drive is known (from arterial blood gas analysis), oxygen should be judiciously controlled to achieve an oxygen saturation (based on pulse oximetry) between 88% and 92%. In this ‘Goldilocks’ zone, the patient will not die of hypoxia and ventilation is unlikely to be depressed to any significant degree.