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Respiratory Medicine. Stephen J. Bourke
Читать онлайн.Название Respiratory Medicine
Год выпуска 0
isbn 9781119774235
Автор произведения Stephen J. Bourke
Жанр Медицина
Издательство John Wiley & Sons Limited
Effect on arterial CO2 content
Blood with a high CO2 content returning from low‐V/Q areas mixes with blood with a low CO2 content returning from high‐V/Q areas. The net CO2 content of arterial blood may be near normal, as the two balance out.
Effect on arterial O2 content
Here the situation is different. Blood returning from low‐V/Q areas has a low PO2 and low O2 content, but there is a limit to how far this deficit can be made good by mixture with blood returning from high‐V/Q areas. Blood returning from a high‐V/Q area will have a high PO2 but is unable to carry more than the ‘normal’ quantity of oxygen, as the haemoglobin will already be saturated.
Areas of low V/Q result in a rise in arterial CO2 and a fall in arterial O2 content.
Increased ventilation in areas of high V/Q may balance the effect on CO2 content but will only partially correct the reduction in O2 content; a degree of hypoxaemia is inevitable.
It follows that, where arterial oxygen levels are lower than would be expected from consideration of PaCO2 (overall ventilation) alone, there must be a disturbance to the normal V/Q matching system in the lung; that is, there is likely to be an intrinsic problem with the lung or its vasculature.
When interpreting arterial blood gas results, it is often important to know whether an observed low PaO2 can be explained by underventilation alone or whether a problem with the lung or pulmonary vasculature is present. The tool we use for this task is the alveolar gas equation.
The alveolar gas equation
An understanding of the relationship between PaCO2 and PaO2 is critical to the interpretation of blood gases (see Chapter 3). The relationship can be summarised in an equation known as the alveolar gas equation.
Pure underventilation leads to an increase in PaCO2 and a ‘proportionate’ fall in PaO2. This is known as type 2 respiratory failure.
A disturbance in V/Q matching leads to impaired gas exchange with a fall in PaO2 but no change in PaCO2. This is known as a type 1 respiratory failure.
Because these two problems can occur simultaneously, the alveolar gas equation is needed to determine whether an observed fall in PaO2 can be accounted for by underventilation alone or whether there is also an intrinsic problem with the lungs (impairing gas exchange).
Rather than merely memorise the alveolar gas equation, spend just a moment here understanding its derivation (this is not a rigorous mathematical derivation, merely an attempt to impart some insight into its meaning).
Imagine a lung, disconnected from the circulation, being ventilated. Clearly, in a short space of time, PAO2 will come to equal the partial pressure of oxygen in the inspired air (PIO2):
In real life, the pulmonary circulation is in intimate contact with the lungs and is continuously removing O2 from the alveoli. The alveolar partial pressure of O2 is therefore equal to the partial pressure in the inspired air minus the amount removed.
If the exchange of oxygen for carbon dioxide were a 1:1 swap then the amount of O2 removed would equal the amount of CO2 added to the alveoli and the equation would become:
The CO2:O2 exchange, as already discussed, is, however, not usually 1:1. The RQ is usually taken to be 0.8.
Thus:
As CO2 is a very soluble gas, PACO2 is virtually the same as PaCO2. PaCO2 (available from the blood gas measurement) can therefore be used in the equation in place of PACO2:
This is (the simplified version of ) the alveolar gas equation. If PIO2 is known then PAO2 can be calculated.
But, so what? What do we do with the PAO2?
Unlike in the case of CO2, there is normally a difference between alveolar and arterial PO2 (which should be the greater?). The difference PAO2 − PaO2 is often written PA–aO2 and is known as the alveolar–arterial (A–a) gradient. In healthy young adults, breathing air, this gradient is small; it would be expected to be comfortably less than 2 kPa. If the gradient is greater than this then the abnormality in the blood gas result cannot be accounted for by a change in ventilation alone; there must be an abnormality intrinsic to the lung or its vasculature causing a disturbance of V/Q matching. For examples, see the multiple choice questions at the end of the chapter.
The control of breathing
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.