OH ccllular CD2 HCO10

and secreted in the peritubular capillaries. The generation of new HCO 3- takes a few days to complete and leads to a further increase in HCO3- with a consequent rise in pH.

In vivo, in this chronic situation, an increase of 10 mmHg (1.33 kPa) in PCO2 above 40 mmHg (5.33 kPa) leads to an increase in plasma HCO3- of approximately 3.5 mmol/l. The increase in HCO3- in respiratory failure is due to two mechanisms: buffering by A--AH buffer pairs, and generation of new HCO3- by tubular cells.

Acid-base regulation in critically ill patients

Every step of acid-base regulation may be affected in critically ill patients.

1. The acid load may be altered by both the underlying disease (hypoperfusion, shock, increased metabolism, etc.) and therapeutic intervention (excessive parenteral feeding).

2. The buffer system is frequently abnormal in critically ill patients; decreased levels of hemoglobin, the most important component of the A --AH buffer pair, are not unusual. A decreased concentration of both A--AH and HCO3--CO2 buffer pairs implies a greater change in pH for a given acid load.

3. Transport of blood from the venous to the arterial side may also be affected (low-flow states). In these conditions the CO 2 clearance may be altered, resulting in a large difference between the acid-base status of the venous and arterial blood, with increases in the PCO2 and pH gradients.

4. The physiological response to increased PCO2 and decreased pH, i.e. increased ventilation, is usually impaired in critically ill patients for two main reasons: the underlying disease may affect the lung, thus preventing increased ventilation, and these patients are usually on mechanical ventilation. If volume-controlled ventilation is used, PCO2 will rise as the patient (usually sedated and sometimes paralyzed) cannot change either the tidal volume or the respiratory rate. If pressure-support ventilation is used, the patient may respond to the increase in PCO2 by triggering mechanical breathing more frequently. However, the depth of breath (i.e. the tidal volume) is often out of the patient's control. Thus it is obvious that mechanical ventilation has a deleterious effect on the physiological response to changes in acid-base status.

5. The physiological response to decreased pH in the renal tubular cells, in which HCO 3- losses are replaced, may also be impaired in the critically ill, whose renal function is often affected. It is also important to realize that some forms of renal support, as hemofiltration, may lead to HCO 3- losses, with consequent additional derangement of the acid-base balance.

In summary, it is important to remember that the physiological control of the acid-base equilibrium is often impaired in critically ill patients, and physicians must understand which mechanisms are altered so that an adequate substitute can be provided for the physiological control which has been lost.

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