METABOLIC ACID–BASE DISORDERS
Metabolic acid–base disorders lead to an accumulation or a loss of H+ resulting in changes in the concentration of HCO3– in the blood. The direct loss or gain of HCO3– will also cause a metabolic acid–base disorder. Thus metabolic disorders are recognized by investigating the concentration of HCO3– in the blood. Respiratory compensation occurs quickly, often within hours, and patients will show some change in blood PCO2 because of hypo-or hyperventilation.
Metabolic acidosis may arise from an increase in the amount of H+ formed or a decrease in the concentration of HCO3–. Diabetic ketoacidosis , lactic acidosis, poisoning with, for example, salicylate, methanol, ethylene glycol or the condition known as inherited organic acidosis all increase the production of H+. In contrast, a decreased excretion of H+ as in renal tubular acidosis, acute and chronic renal failure , the use of inhibitors of carbonic anhydrase or a deficiency of mineralocorticoid, such as aldosterone (Figure 9.8) all increase blood H+ content. Acid ingestion, as in acid poisoning, the excessive intake of amino acids by infusion, the direct loss of HCO3– by diarrhea or a pancreatic fistula can all reduce the concentration of HCO3– in the blood.
The clinical effects of metabolic acidosis include hyperventilation, where the increased H+ concentration acts as a rapid and powerful stimulant of the respiratory center leading to a deep sighing breathing called Kussmaulrespiration. The patients may also present with neuromuscular irritability thatcan cause cardiac arrhythmias. Cardiac arrest is more likely in the presence of hyperkalemia. Eventually metabolic acidosis can depress the activities of the central nervous system and this can progress to coma and even death. Patients with metabolic acidosis are managed by treating the underlying cause and this usually resolves the acid–base disorder. In severe cases, the patients may be administered HCO3– intravenously to correct the acidosis.
Metabolic alkalosis may occur as a consequence of gastrointestinal loss of H+ following vomiting and gastric aspiration or from excessive renal loss of H+ in Conn’s and Cushing’s syndromes . Some clinical treatments, such as the use of carbenoxolone, an anti-inflammatory drug used to treat ulcers, and thiazide diuretic drugs that reduce blood pressure by promoting the secretion of urine and by K+ depletion, can also result in this condition. Finally, the administration of alkali, including alkali ingestion, and inappropriate treatment for acidosis can also cause metabolic alkalosis.
The clinical effects of metabolic alkalosis include hypoventilation that is a consequence of the low H+ concentration. It is often accompanied by mental confusion and eventually coma. Patients may also suffer from paresthesia. Other effects of metabolic acidosis include tetany and muscle cramps that arise due to a decrease in the concentration of unbound Ca2+ in the plasma arising from the alkalosis. Metabolic alkalosis is usually managed by treating its underlying cause.