Oxygen transport

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Oxygen transport

Normal oxygen transport

The total blood oxygen content is the sum of the dissolved oxygen and that bound to haemoglobin. Only a small fraction (2%) of the total oxygen in blood is in solution, and this dissolved oxygen is directly proportional to the arterial PO₂. The arterial PO₂ is also an important factor affecting the amount of oxygen that is bound to haemoglobin, as oxyhaemoglobin. The relationship is shown in the oxygen–haemoglobin dissociation curve (Fig 23.1).

Fig 23.1 Dissociation curves – the relationship between PO₂ and oxygen binding to haemoglobin. (a) The normal oxygen haemoglobin dissociation curve. (b) The effect of 50% CO.

Measurement of blood oxygen saturation, the percentage of the total haemoglobin present as oxyhaemoglobin, may be used to assess the ability of blood to carry oxygen to the tissues. This clearly depends on the relative amounts of both oxygen and haemoglobin, as well as their ability to bind together. Delivery of oxygen to the tissues also depends on blood flow, which is in turn influenced by other factors (Table 23.1).

Table 23.1

Factors affecting the delivery of oxygen to the tissues

Blood oxygen content

Haemoglobin concentration

Haemoglobin function

Blood flow

Peripheral perfusion

When arterial PO₂ is high (above 10 kPa), the blood haemoglobin is almost fully saturated with oxygen and measurements of oxygen saturation are not normally required. Indeed, measurements of oxygen saturation are not widely available outside of intensive therapy units. In patients exposed to carbon monoxide following smoke inhalation, the PO₂ may give a misleading indication of the amount of oxygen being carried in the blood because carbon monoxide binds to haemoglobin with greater affinity than does oxygen (Fig 23.1).

When metabolic needs exceed the supply of oxygen, cells switch to anaerobic glycolysis to provide ATP, and produce lactic acid. Measurement of serum lactate concentration can provide additional evidence of the adequacy of tissue oxygenation.

In practice, tissue perfusion is more important than blood oxygen content in ensuring that aerobic metabolism can continue.

Respiratory failure

Figure 23.2 shows how the partial pressures of oxygen and carbon dioxide change as blood flows to the tissues and returns to the lungs. The mechanical process of moving air into and out of the respiratory tract is called ventilation. Carbon dioxide diffuses through alveolar membranes much more efficiently than oxygen, even though there is only a small pressure gradient. The PCO₂ of arterial blood is thus identical to the PCO₂ within the alveoli, and the arterial PCO₂ is therefore a measure of alveolar ventilation. If ventilation is impaired, alveolar PO₂ falls and alveolar PCO₂ rises. Arterial blood reflects these changes. The main chemical stimuli to ventilation are shown in Table 23.2.

Table 23.2

Chemical stimuli to ventilation

Carbon dioxide; an increased PCO₂ is the most important stimulus

[H⁺]: a rise in hydrogen ion concentration stimulates ventilation; in respiratory disease [H⁺] and PCO₂ rise together

Oxygen: a decreased PO₂ increases ventilation, but is of less importance unless PO₂ falls below 8 kPa

Fig 23.2 Normal gas pressures are maintained by ventilation and gas exchange.

It is possible to calculate the alveolar–arterial PO₂ gradient to determine the extent of defective gas exchange (Fig 23.3), but in practice it is rarely necessary to do this.

Fig 23.3 How to calculate the alveolar–arterial PO₂ difference.

An arterial PO₂ less than 8.0 kPa in a patient breathing room air at rest is known as ‘respiratory failure’. Classically, hypoxia with carbon dioxide retention is called type 2 respiratory failure. Hypoxia without carbon dioxide retention is type 1 respiratory failure.

Two processes contribute to the blood gas pattern in those patients with hypoxia, where PCO₂ is not elevated (type 1 respiratory failure). These are:

impaired diffusion

ventilation/perfusion imbalance.

Impaired diffusion

Here the presence of fluid, as in pulmonary oedema, or thickened alveolar walls, such as occurs in pulmonary fibrosis, inhibits oxygen diffusion, although carbon dioxide passage is more readily accomplished. PO₂ is low but PCO₂ may be within reference limits.

Ventilation/perfusion imbalance

In patients with a lobar pneumonia, some of the blood perfusing the lungs does not come into contact with functional alveoli and retains its carbon dioxide, and is not oxygenated. In blood reaching other parts of the lungs, gas exchange takes place efficiently. Arterial blood is a mixture of that exiting both regions. The increased PCO₂ stimulates ventilation and ensures that the functioning alveoli are worked harder to restore PCO₂ to normal. The blood gas results will show normal or even low PCO₂ as a result of this hyperventilation (Fig 23.4). However, increased ventilation cannot dramatically raise alveolar PO₂ as long as the patient is breathing air.

Fig 23.4 Blood gases in (a) normal circumstances, (b) hypoventilation and (c) where there is a ventilation/perfusion imbalance.

Blood passing from the right side of the heart directly to the arterial circulation without being exposed to the inspired gas in the ventilated alveoli is an extreme example of ventilation/perfusion imbalance. This right to left ‘shunting’ occurs in cyanotic congenital heart disease.

Hypoxia with raised PCO₂ (type 2 respiratory failure) indicates diminished ventilation and impaired gas exchange, and may be seen in patients with bronchial pneumonia or chronic bronchitis.

Oxygen therapy

In all respiratory diseases, oxygen therapy is a vital aspect of patient management but there is one caution. Some patients with chronic bronchitis become insensitive to respiratory stimulation by carbon dioxide. This insensitivity may develop over many years, and only the existing hypoxia keeps respiration going. Treating such patients with high concentrations of oxygen only serves to reduce respiration further. PCO₂ rises, acidosis worsens and the patient may become comatose.

Clinical note

Pulse oximetry is an accurate non-invasive way of assessing oxygen saturation. Oxygenated and reduced haemoglobin absorb light at different wavelengths. If light of these wavelengths is passed through a blood vessel, the proportion of oxygenated haemoglobin can be calculated. Pulse oximetry allows these measurements in ‘pulsing’ blood only, producing results that approximate to arterial values.

Case history 17

A 58-year-old man was admitted with a history of chronic obstructive airways disease for many years. On examination he was cyanosed, breathless and there was marked systemic oedema. A blood sample gave the following results:

Arterial blood gases:

• Describe the acid–base disorder.

• What type of respiratory problem is present?

Comment on page 165.

Oxygen transport

Oxygen is carried in blood mostly bound to haemoglobin. Arterial blood PO₂ determines how much oxygen is bound to haemoglobin, although above a PO₂ of 10 kPa the haemoglobin is usually fully saturated.

Measurements of haemoglobin and blood oxygen saturation are necessary to assess oxygen availability where the patient is anaemic, or if factors affecting the ability of the haemoglobin to bind oxygen, such as carbon monoxide, are present.

Delivery of oxygen to the tissues also depends on cardiac output and peripheral perfusion.

Respiratory failure is defined as an arterial PO₂ of less than 8 kPa in a patient breathing air.

Hypoxia with CO₂ retention is seen where there is impaired ventilation.

Hypoxia without CO₂ retention is seen commonly when there is ventilation/perfusion imbalance.

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