TAILIEUCHUNG - Chapter 048. Acidosis and Alkalosis (Part 11)

Alkali Administration Chronic administration of alkali to individuals with normal renal function rarely, if ever, causes alkalosis. However, in patients with coexistent hemodynamic disturbances, alkalosis can develop because the normal capacity to excrete HCO3– may be exceeded or there may be enhanced reabsorption of HCO 3–. Such patients include those who receive HCO3– (PO or IV), acetate loads (parenteral hyperalimentation solutions), citrate loads (transfusions), or antacids plus cation-exchange resins (aluminum hydroxide and sodium polystyrene sulfonate). . | Chapter 048. Acidosis and Alkalosis Part 11 Alkali Administration Chronic administration of alkali to individuals with normal renal function rarely if ever causes alkalosis. However in patients with coexistent hemodynamic disturbances alkalosis can develop because the normal capacity to excrete HCO3- may be exceeded or there may be enhanced reabsorption of HCO3-. Such patients include those who receive HCO3- PO or IV acetate loads parenteral hyperalimentation solutions citrate loads transfusions or antacids plus cation-exchange resins aluminum hydroxide and sodium polystyrene sulfonate . Metabolic Alkalosis Associated with ECFV Contraction K Depletion and Secondary Hyperreninemic Hyperaldosteronism Gastrointestinal Origin Gastrointestinal loss of H from vomiting or gastric aspiration results in retention of HCO3-. The loss of fluid and NaCl in vomitus or nasogastric suction results in contraction of the ECFV and an increase in the secretion of renin and aldosterone. Volume contraction through a reduction in GFR results in an enhanced capacity of the renal tubule to reabsorb HCO3-. During active vomiting however the filtered load of bicarbonate is acutely increased to the point that the reabsorptive capacity of the proximal tubule for HCO3 is exceeded. The excess NaHCO3 issuing out of the proximal tubule reaches the distal tubule where H secretion is enhanced by an aldosterone and the delivery of the poorly reabsorbed anion HCO3-. Correction of the contracted ECFV with NaCl and repair of K deficits corrects the acid-base disorder and chloride deficiency. Renal Origin Diuretics See also Chap. 227 Drugs that induce chloruresis such as thiazides and loop diuretics furosemide bumetanide torsemide and ethacrynic acid acutely diminish the ECFV without altering the total body bicarbonate content. The serum HCO3- increases because the reduced ECFV contracts the HCO3- in the plasma contraction alkalosis . The chronic administration of diuretics tends to generate an alkalosis

• Y học thường thức
• Acidosis and Alkalosis
• bệnh học và điều trị
• bài giảng bệnh học
• tài liệu học ngành y
• Harrisons Internal Medicine
• Respiratory acidosis
• Respiratory alkalosis
• Metabolic acidosis
• Arterial blood gas interpretation
• Metabolic alkalosis
• Compensatory mechanisms
• BMC Pharmacology and Toxicology
• Airway surface liquid pH
• Airway blood flow
• Blood gases
• Case examples
• medical books
• pharmacology
• epidemiologic
• Obstetrics
• anatomy
• Preventing Morbidity
• Multidisciplinary Care
• Handbook of blood gas
• Base interpretation
• Buffer systems
• Carbon dioxide levels
• Gas exchange
• The non invasive monitoring
• Clinical approach
• Diagnose acid–base disorders
• Drinking binge yesterday