Introduction

Metabolic alkalosis is the most frequently observed acid-base abnormality in hospital patients and in postoperative patients. In a study of 13 430 acid-base analyses, it has been identified in 40 per cent of all samples and in 51 per cent of abnormal samples. Metabolic alkalosis causes significant clinical and metabolic complications, and thus deserves early recognition and appropriate management. More detailed discussions are given by Harrington and Kas.sjieií1982), JacobsonjndSeldin

(1983), s.a.ba.tj.oj., ..aod., ...Ku.rtzm.§.D,..il994), and Gail_a_il9_95). Definitions

The term alkalosis refers to the abnormal processes tending to decrease the amount of acid or to increase the amount of alkali in the organism, and thus to increase blood pH. Respiratory alkalosis results from a primary decrease in PaCO2, and metabolic alkalosis from a primary increase in bicarbonate concentration. Alkalemia refers to a blood pH value above 7.45, regardless of its mode of generation.

In the normal subject, acidosis and alkalosis elicit an adaptative response with tends to bring the pH back to its normal value ( Table 1). Metabolic alkalosis causes a decrease in ventilation and an increase in PaCO2. Reference to this secondary change as respiratory acidosis should be avoided because it is a normal compensatory response and not an abnormal process due to respiratory dysfunction.

Table 1 Normal compensatory responses to primary acid-base disturbances

Compensatory responses are essentially proportional to the primary acid-base disturbance and are effective in limiting the change in pH. However, two points should be kept in mind. First, respiratory responses are rapid and reach their maximum within hours, whereas renal responses are complete after only 3 to 5 days. For example, if PaCO2 rises to 70 mmHg, arterial blood pH first decreases to 7.20 (acute condition) and then progressively increases to reach 7.32 (chronic condition). Therefore the recent history must be taken into account for the correct assessment of compensation. Second, although compensatory responses limit the change in pH, they do not bring the pH back to normal. A pH of 7.40 in a patient with chronic hypercapnia of 70 mmHg should not be interpreted as an appropriate response because of the so-called normal pH, but as a superimposed metabolic alkalosis. Similarly, 'overcompensation' does not occur and must be interpreted as indicating the presence of another acid-base disturbance.

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