Respiratory Medicine. Stephen J. Bourke

able to distinguish between these two very different mechanisms.

      Transfer coefficient (KCO) is the transfer factor divided by V_A. This tells us the transfer factor ‘per unit lung volume’. Like T_LCO, KCO is reduced when there is intrinsic lung disease, but unlike T_LCO, KCO is not diminished when a healthy lung is reduced in volume by some external factor.

      Interpretation

      In restrictive conditions, a reduced KCO suggests an intrapulmonary cause (e.g. fibrosis). In extrapulmonary causes (e.g. chest wall deformity, respiratory muscle weakness, obesity), the KCO tends to be elevated. (Reason: KCO is effectively telling us about the transfer of CO only in the alveoli that are ventilated. The non‐ventilated alveoli are effectively discounted because they don’t contribute to V_A. As the V/Q matching system will divert blood away from the non‐ventilated alveoli, the ventilated alveoli will have more than their normal share of blood. The greater blood volume increases CO absorption and thus gas transfer.)

      In obstructive conditions, a reduced KCO suggests COPD (emphysema). In asthma, the KCO may be elevated. (Reason: Asthma does not affect every airway to an identical degree; there is therefore an exaggerated heterogeneity of ventilation. As discussed already, KCO is more heavily influenced by the well‐ventilated areas which, because of V/Q matching, have more than their fair share of perfusion.)

      In the presence of normal spirometry, a reduced KCO is a strong indicator of intrinsic lung disease (affecting the pulmonary vasculature or alveoli; consider pulmonary hypertension or a combination of emphysema and fibrosis). (Reason: the effects of emphysema and fibrosis on FEV₁:FVC ratio cancel each other out though both cause a diminution in gas transfer.)

Arterial blood gases

Normal values are listed in Table 3.1.

A sample of arterial blood may be obtained from any artery, but the radial artery at the wrist and the brachial artery in the antecubital fossa are the sites most commonly used. The blood enters the heparinised needle and syringe under its own pressure with a pulsatile action. The syringe containing the arterial blood is capped, placed in ice and analysed in the laboratory within 30 minutes of sampling.

      Review of acid/base balance

      CO₂ dissolves in H₂O and forms carbonic acid (H₂CO₃), which dissociates into H⁺ and HCO₃ ^– in a constant relationship:

Table 3.1 Normal values for arterial blood gases whilst breathing normal room air at sea level

pH	7.35–7.45
PCO 2	4.5–6.0 kPa, 34–45 mmHg
PO 2	11–14 kPa, 83–105 mmHg
Actual bicarbonate (aHCO 3 – )	22–26 mmol/L
Standard bicarbonate (sHCO 3 – )	22–26 mmol/L
Base excess	–2 to +2 mmol/L
Oxygen saturation	96–98%

      Thus:

      As [H₂CO₃] directly relates to the partial pressure of CO₂:

      In other words, for a given concentration of bicarbonate, PCO₂ has a direct linear relationship with [H⁺] (and thus an inverse relationship with pH, which is the negative logarithm of [H⁺]).

      Similarly, for a given PCO₂, there is a direct relationship between [HCO₃ ^–] and pH.

These relationships can be represented graphically (Fig. 3.9).

      Bicarbonate concentration

Most blood gas analysers provide two different measurements of bicarbonate – ‘actual bicarbonate’ and ‘standard bicarbonate’ – in addition to another value, ‘base excess’. This can cause confusion, although it needn’t. The analyser measures the bicarbonate level in the blood sample. This actual measurement is (conveniently) known as the actual bicarbonate (aHCO₃ ^–). As can be seen in Fig. 3.9, the actual level is directly dependent on the PCO₂ (for a given pH: the higher the PCO₂, the higher the aHCO₃ ^–; the lower the PCO₂, the lower the aHCO₃ ^–). What we’d like to know is what the bicarbonate would have been if the PCO₂ had been normal (5.3 kPa) because that gives us a direct handle on ‘what the metabolic system is doing’. If we know the actual bicarbonate (aHCO₃ ^–) and the PCO₂ then we can calculate that value. However, we don’t need to, the machine will do it for us. This calculated bicarbonate value for a ‘standard’ PCO₂ is (conveniently) known as the standard bicarbonate (sHCO₃ ^–). Either aHCO₃ ^– or sHCO₃ ^– can be used in the interpretation of blood gases, but the sHCO₃ ^– takes out the immediate effect of CO₂ on the bicarbonate level and can loosely be regarded as giving a more direct indication of the metabolic activity influencing acid/base balance, (I think it’s easier). The base excess takes into account the fact that there are other buffers apart from bicarbonate in the blood. It tells a similar story to the bicarbonate level in terms of acid/base disturbance. Its principal advantage is the ease with which its normal range can be remembered. As one might anticipate from the name, the ‘excess’ should be zero (normal range is 0±2 mmol/L). There aren’t many numbers easier to remember than zero.

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