2014-18 Metabolic alkalosis associated with ECFV contraction Metabolic alkalosis with ECFV expansion K depletion, and secondary hyperreninemia hyperaldosteronism Mineralocorticoid administration or excess Gastrointenstinal production HCO3 retention volume contraction Symptoms Diuretics Nonreaborbable anions and magnesium Related electrolyte abnormalities: hypokalemia Treatment Correcting the underlying stimulus for HCo3 generation After treatment of lactic acidosis or Removing the factors that sustain HCO reabsorption(ECFV ketoacidosis posthypercapnia Respiratory acidosis Clinical features Severe pulmonary disease, respiratory muscle The clinical feature varies according to fatigue or abnormalities in ventilatory control Severity and duration Acute: immediate compensatory elevation Underlying disease HCO3, which increases 1 mmol/L for every 10 whether there is hypoxemia ty, dyspnea mmHg increase in pCo2 confusion. coma Chronic(>24h): renal adaptation increases the Chronic hypercapnea: sleep disturbances, loss o [HCO3] by 4 mmol/L Treatment Respiratory alkalosis Acute respiratory acidosis HCO3/PCO2 When PaCO2 is 40-15 mmHg, the relationship between measures to reverse the underlying cause should arterial [H+]and Paco2 is about 0.7 mmol/L per mmHg, and be undertaken simultaneously with restoration of of plasma [HCo3]is O adequate alveolar ventilation Hypocapnia sustained longer than 2 to 6 h is further Chronic respiratory acidosis Improving lung function Full renal adaptation may take several days and require normal volume status and renal function 82014-1-8 8 Metabolic alkalosis associated with ECFV contraction, K depletion, and secondary hyperreninemic hyperaldosteronism • Gastrointenstinal – HCO3 retention + volume contraction • Renal origin – Diuretics – Nonreaborbable anions and magnesium deficiency – Potassium depletion – After treatment of lactic acidosis or ketoacidosis – posthypercapnia Metabolic alkalosis with ECFV expansion, hypertension and hyperaldosteronism • Mineralocorticoid administration or excess production • Symptoms: – changes in central and peripheral nervous system function: confusion, obtundation, a predispositin to seizures … • Related electrolyte abnormalities: hypokalemia • Treatment – Correcting the underlying stimulus for HCO3 generation – Removing the factors that sustain HCO reabsorption (ECFV contraction) Respiratory acidosis • Severe pulmonary disease, respiratory muscle fatigue or abnormalities in ventilatory control • Acute: immediate compensatory elevation in HCO3, which increases 1 mmol/L for every 10 mmHg increase in pCO2 • Chronic (>24h): renal adaptation increases the [HCO3] by 4 mmol/L Clinical features • The clinical feature varies according to – Severity and duration – Underlying disease – Whether there is hypoxemia • A rapid increase in pCO2: anxiety, dyspnea, confusion… coma • Chronic hypercapnea: sleep disturbances, loss of memory, .. Treatment • Acute respiratory acidosis – can be life-threatening, – measures to reverse the underlying cause should be undertaken simultaneously with restoration of adequate alveolar ventilation • Chronic respiratory acidosis – Improving lung function Respiratory alkalosis • Alveolar hyperventilation decreases PaCO2 and increases the HCO3/PCO2 • When PaCO2 is 40 – 15 mmHg, the relationship between arterial [H+] and PaCO2 is about 0.7 mmol/L per mmHg, and that of plasma [HCO3] is 0.2 mmol/ per mmHg • Hypocapnia sustained longer than 2 to 6 h is further compensated by a decrease in renal ammonium and titratable acid excretion. • Full renal adaptation may take several days and require normal volume status and renal function