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Q1: What is the diagnosis on admission? What other electrolyte result is essential in management of this condition?
The patient has metabolic alkalosis. Serum chloride is essential for further management. The chloride was measured at <70 mmol/l, the lowest point at which the assay is accurate and was probably considerably lower than this.
Q2: Explain the effect of supplemental oxygen on the arterial blood gas result(point A to point B; see fig 1 on p 242)
Increasing the inspired oxygen has improved the oxygenation; however, the carbon dioxide and bicarbonate have risen further. This is because compensation for metabolic alkalosis involves hypoventilation, leading to respiratory acidosis. The degree of hypoventilation is limited by hypoxia and by providing a higher inspiratory concentration of oxygen a further decrease in minute ventilation has occurred. This has resulted in a rise in carbon dioxide.
Q3: Explain the action of saline (point B to point C) and acetazolamide (point C onwards; see fig 1 on p 242)?
This patient’s alkalosis is due to a loss in hydrochloric acid from the gut during the severe and protracted vomiting. For every hydrogen ion secreted into the gut a bicarbonate ion is released into the serum. Potassium chloride is also lost into the gut. The resulting dehydration and hypokalaemia leads to increased sodium reabsorption from the kidney. Unfortunately there is no chloride available to accompany the sodium, therefore to maintain electrochemical neutrality hydrogen ions and potassium ions are lost from the kidney. This continued loss of hydrogen ions maintains the alkalosis. Saline provides rehydration and chloride ions, which enable the kidney to conserve hydrogen, thereby improving the alkalosis.
Acetazolamide acts by inhibiting carbonic anhydrase in the kidney, thereby promoting bicarbonate loss.
Q4: What is the cause of her hypoxia at point D (see fig 1 on p 242)? How could this have occurred?
The chest radiograph (see fig 2 on 242) shows a collapsed left lung, probably caused by hypoventilation and subsequent mucus plugging.
Metabolic alkalosis develops when a net acid loss or net base gain is associated with a failure of excretion of bicarbonate by the kidney. The condition has three phases: generation, maintenance, and correction.
The generation of metabolic alkalosis occurs in one of two ways. Firstly, loss of acid, for example in gastric fluid and urine or because of acid shift into cells. Second, serum bicarbonate can rise inappropriately, for example with exogenous bicarbonate administration or in post-hypercapnic states when continued reabsorption of bicarbonate can occur for some days.
Maintenance of the alkalosis may be by the same or a different mechanism, common causes being volume depletion, hypokalaemia, mineralocorticoid excess, hypochloraemia, and a reduced glomerular filtration rate.
Clinically the condition is grouped into a chloride responsive type and a chloride resistant type. The chloride responsive type is associated with volume depletion and may be due to persistent loss of gastric acid, diuretic use, diarrhoea, high doses of penicillin, or in post- hypercapnic states. The chloride resistant type is associated with a normal or expanded extracellular fluid volume, may be due to hyperaldosteronism, excess alkali intake, or hypoproteinaemia.
Clinically the patient may exhibit confusion, apathy, and stupor. Rarely generalised twitching, tetany, and coma are seen. There may be hypoventilation with reduced respiratory rate and depth. Cardiac dysrrhythmias may occur. Serious ventricular dysrrhythmias may appear if the pH is >7.5 and are related to severe hypokalaemia. Features of volume contraction may be prominent and investigations may show an increase in urea, creatinine, and packed cell volume. Abdominal distension may occur secondary to ileus.
The symptoms of metabolic alkalosis per se are difficult to separate from those of chloride, volume, or potassium depletion. Compensatory hypoventilation may cause hypoxia and contribute to pulmonary infection in critically ill patients. Blood gas measurements provide the definitive diagnosis.
Management of the alkalosis depends on the cause. If the dehydration is the primary mechanism it should be corrected, along with potassium and magnesium deficits. Primary mineralocorticoids excess may be treated with spironolactone before definitive therapy. In patients with post-hypercapnic metabolic alkalosis acetazolamide will result in a prompt bicarbonate diuresis. Ammonium chloride or arginine hydrochloride infusion into large vein over 18–24 hours may be useful in resistant cases. Finally, in patients with renal failure or precarious fluid status haemodialysis allows precise control of fluid regulation.
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