Clinical manifestations

The compensatory response to metabolic alkalosis is a decrease in ventilation and an increase in PaCO2. Multiple cases of severe hypercapnia that are clearly due to metabolic alkalosis have been reported. Whether the response is or is not always present, and whether its magnitude depends on the cause of the alkalosis or on associated factors, has been questioned in numerous studies. It is now accepted that the increase in PaCO2 is proportional to the increase in bicarbonate concentration and is independent of the mode of generation of the alkalosis. PaCO2 normally increases by about 0.7 mmHg for each increase of 1 mmol/l in bicarbonate concentration and can exceed 80 mmHg (10.7 kPa) in severe cases. Hypoxemia is almost always present, and has generally been attributed to the decreased ventilation and the resulting atelectasis. Metabolic alkalosis also inhibits hypoxic pulmonary vasoconstriction, which contributes to the deterioration of pulmonary gas exchange and to increasing hypoxemia in patients with respiratory failure ( Brimlipui!e 1991).

Cardiovascular complications mainly consist of various cardiac arrhythmias: supraventricular and ventricular premature beats, supraventricular tachycardia, atrioventricular block, ventricular tachycardia, and fibrillation. The arrhythmias seem to result from the associated potassium depletion rather than from the increase in pH, and are enhanced by myocardial ischemia and digitalis therapy. Alkalosis has a small positive inotropic effect, at least in animal studies.

Neurological complications generally consist of altered orientation and comportment, decreased consciousness, and neuromuscular hyperexcitability. Coma and grand mal seizures may occur, but are generally precipitated by concomitant hypovolemia, hypercapnia, hypoxemia, or other metabolic disturbances (e.g. hyperammonemia in hepatic failure). Muscle weakness may occur in the presence of severe potassium depletion.

Alkalosis shifts the oxyhemoglobin dissociation curve to the left, thereby increasing oxygen uptake in the lung and decreasing oxygen release to peripheral tissues. Alkalosis also increases red cell 2,3-diphosphoglycerate concentration, which has an opposite effect and returns the dissociation curve to its original position after 6 to 8 h. Alkalosis increases the oxygen consumption, and increases the blood lactate concentration by a pH-induced enzymatic activation. Potassium depletion is almost invariably present in metabolic alkalosis and contributes to its clinical manifestations. Calcium concentration is typically normal, and the hyperexcitability results from decreased calcium ionization or an associated magnesium depletion. Alkalosis enhances the conversion of the ammonium ion to ammonia.

Mixed acid-base disorders are common in critically ill patients and should be actively sought. Particular attention should be paid to the combination of respiratory acidosis and metabolic alkalosis, which is very common but frequently misdiagnosed when the resulting pH remains close to 7.40. Spontaneous correction is unlikely, since each disturbance contributes to enhance the other. Metabolic alkalosis may cause serious alkalemia when the patient is mechanically ventilated, and serious hypercapnia and hypoxemia when weaning is attempted.

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