Emergency Medicine

ACID–BASE DISTURBANCES

128 Acid–Base, Electrolyte and Renal Emergencies

(i) The acidosis is partially compensated if the PaCO 2 value is higher

than predicted.

(ii) A primary respiratory alkalosis coexists if the PaCO 2 value is

lower than predicted.

6 There are few specific clinical features due to an acute metabolic acidosis

itself, other than hyperventilation known as Kussmaul breathing.

7 Urea and electrolytes (U&Es) confirm a primary fall in plasma bicarbonate

below 22 mmol/L and usually show an associated rise in plasma potassium

from an extracellular shift.

MANAGEMENT

1 Provide supportive treatment with oxygen, i.v. f luids and treat symptomatic

hyperkalaemia (see p. 132).

2 Correct any reversible underlying disorder:

(i) Administer fluid and insulin, and replace potassium in diabetic

ketoacidosis.

(ii) Ensure adequate oxygenation and restore the intravascular

volume to improve peripheral perfusion in lactic acidosis.

3 Refer the patient to the medical team. Dialysis will be necessary for renal

failure and severe methanol or salicylate poisoning.

Metabolic alkalosis

DIAGNOSIS

1 An abnormal process or condition leading to a serum bicarbonate level of

>28 mmol/L.

2 Causes include:

(i) Addition of base to extracellular fluid:

(a) recovery from organic acidosis secondary to metabolism of

lactate and acetate

(b) milk-alkali syndrome

(c) massive blood transfusion (metabolism of citrate).

(ii) Chloride depletion:

(a) loss of gastric acid from vomiting or gastric aspiration

(b) diuretics.

(iii) Potassium depletion:

(a) primary (Conn’s) and secondary hyperaldosteronism

(b) Cushing’s or Bartter’s syndromes

(c) severe hypokalaemia.

(iv) Other:

(a) laxative abuse

(b) severe hypoalbuminaemia.