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acid base balance.ppt

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acid base balance.ppt

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acid base balance.ppt

  1. 1. Approach to Acid-Base Disorders Name : zayed abukoosh Group : 1877
  2. 2. Regulation of plasma HCO3 - • Via kidneys: 1. Reabsorption of filtered HCO3 2. Formation of titratable acid 3. Excretion of NH4 + in urine
  3. 3. Maintenance of blood pH • Maintenance of the ratio of HCO3 to pCO2 via compensatory responses by the kidneys and lungs • Chemical buffering: – includes HCO3, phosphates, proteins, hemoglobin, bone carbamates
  4. 4. Determinants of AG Unmeasured Anions Unmeasured Cations Albumin (15mEq/L) Calcium (5 mEq/L) Organic Acids (5 mEq/L) Potassium (4.5 mEq/L) Phosphate (2 mEq/L) Magnesium (1.5 mEq/L) Sulfate (1 mEq/L) ---------------------------- --------------------------- Total UA (23 mEq/L) Total UC (11 mEq/L) AG = UA – UC = 12 mEq/L
  5. 5. Metabolic Acidosis May be due to: – Increased endogenous acid production (e.g. lactate and ketones) – Loss of bicarbonate (e.g. diarrhea) – Decreased excretion of endogenous acids (e.g. renal failure)
  6. 6. Metabolic Acidosis CLINICAL EFFECTS • Kussmaul breathing, dyspnea • Headache, nausea, vomiting, confusion, stupor, coma • Decreased myocardial contractility and response to catecholamine; peripheral vasodilatation with central vasoconstriction predisposing to pulmonary edema; arrhythmia
  7. 7. Metabolic Alkalosis PATHOGENESIS • Due to net gain of HCO3 or loss of volatile acid (usually HCl by vomiting) • 2 stages: – GENERATIVE STAGE: loss of acid – MAINTENANCE STAGE: failure of kidneys to compensation by excreting HCO3, because of volume contraction, low GFR, or depleted K+ or Cl-
  8. 8. Metabolic Alkalosis CLINICAL EFFECTS • increases the affinity of hemoglobin for oxygen -- --- decrease tissue unloading • Decreases ventilation • Decreases ionized calcium ----- neuromuscular hyperirritability • Supraventricular and ventricular arrhythmias
  9. 9. Metabolic Alkalosis MANAGEMENT • Identify and correct the underlying stimulus for HCO3 generation • Remove the factors that sustain HCO3 reabsorption (e.g. ECF contraction or hypoK+) • Acetazoleamide • Dilute 0.1N HCl or NH4Cl • Hemodialysis
  10. 10. Respiratory Acidosis ETIOLOGY and PATHOGENESIS • may be due to severe pulmonary disease (e.g. advanced COPD), respiratory muscle fatigue, or abnormalities in ventilatory control (e.g. stroke)
  11. 11. Respiratory Acidosis CLINICAL EFFECTS • depends on severity and acuteness • may be dyspneic or tachypneic • Systemic vasodilation especially cerebral vasodilation ----- increased ICP ----- pseudotumor cerebri • Myoclonic jerks, asterixis, tremors, restlessness, coma
  12. 12. Respiratory Acidosis MANAGEMENT • Depends on severity and rate of onset • May be life-threatening • Measures to reverse underlying cause • Restoration of adequate alveolar ventilation • Avoid rapid correction of hypercapnea
  13. 13. Respiratory Alkalosis ETIOLOGY and PARTHENOGENESIS • Develops when a sufficiently strong ventilator y stimulus causes CO2 output in the lungs to exceed its metabolic production in the tissues • May be due to stimulation of CNS (e.g. pain, anxiety), peripheral chemo receptors (e.g. hypooxemia to pneumonia), chest receptors .
  14. 14. Respiratory Alkalosis CLINICAL EFFECTS • Panic, weakness, and sense of impending doom • Paresthesias about the hands and feet • Possible tetany, seizures
  15. 15. Interpretation of Acid - Base Disorders • Determine if sample is arterial or venous. • Compare HCO3 on ABG and electrolyte panel to verify accuracy • Determine if pH or pCO2 are normal or abnormal. • If any of above are abnormal determine primary A-B disturbance • Compute for expected compensation to determine presence of mixed disorders.

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