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Aproach to the patient with acid - base disorders

Zehra Eren,M.D. Aproach to the patient with acid - base disorders. LEARNING OBJECTIVES. recall normal acid-base balance recall buffer systems in regulation of pH recall Henderson-Hasselbach Equation describe metabolic acidosis and alkalosis describe respiratory acidosis and alkalosis

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Aproach to the patient with acid - base disorders

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  1. Zehra Eren,M.D. Aproachtothepatientwithacid-basedisorders

  2. LEARNING OBJECTIVES • recall normal acid-base balance • recall buffer systems in regulation of pH • recall Henderson-Hasselbach Equation • describe metabolic acidosis and alkalosis • describe respiratory acidosis and alkalosis • manage acid-base disorders

  3. LEARNING OBJECTIVES "Life is a struggle, not against sin, not against the Money Power, not against malicious animal magnetism, but against hydrogen ions." H.L. MENCKEN

  4. Normal Acid-Base Balance • Daily net acid production:1mEq hydrogen ions (H+) per kilogram • H+: 0.0004 mEq/L (40nmol/L)= pH: 7.40 • Arterial pH:7.35-7.45 • İntracellular pH:7.0-7.3

  5. Buffer Systems in Regulation of pH • Extracellular fluid: - bicarbonate ion (HCO3-) /carbonic acid H++HCO3-⇔ H2CO3 H2O + CO2 - plasma proteins - phosphate ions - Ca2+ and HCO3-release of bone carbonic anhydrase

  6. Buffer Systems in Regulation of pH • İntracellular fluid - hemoglobin - cellular proteins - organophosphate complexes - HCO3- by the H+/ HCO3-transport mechanism

  7. Henderson-HasselbachEquation • pH=6.1+log pH 7.00 7.40 7.70 [H+]nmol/L 100 40 20 [HCO3-] (mEq/L) 0.03XpCO2 (mm Hg)

  8. Normal Levels • pH: 7.35-7.45 • pCO2: 37-45 mmHg • HCO3- : 22-26 mEq/L

  9. pH • Acidosis <7.35-7.45> Alkalosis • HCO3-↑↓ → Metabolic • CO2 ↑↓ → Respiratory

  10. Compensatory response to acid-base disorders • Metabolic Acidosis/Alkalosis→ reducing / increasing CO2 • Respiratory Acidosis/Alkalosis→ renal secretion / reabsorption of HCO3-/H+

  11. Metabolic Acidosis • Fall in HCO3- concentration with fall in pH • Compensatory response: fall in pH causes increased respiration, reducing CO2 • 1.2 mmHg fall in arterial PCO2 for every 1 meq/L reduction in the serum HCO3 concentration

  12. Formulas • Arterial PCO2 = 1.5 x serum HCO3 + 8 ± 2 (Winters’ equation) • Arterial PCO2 = Serum HCO3 + 15 • Arterial PCO2 should be similar to the decimal digits of the arterial pH (eg, 25 mmHg when the arterial pH is 7.25, a setting in which the serum HCO3 concentration would be approximately 11 meq/L)

  13. Causes of Metabolic Acidosis • İncreases acid load (H+) • HCO3- loses - extrarenal: gastrointestinal - renal

  14. Plasma Anion Gap • [Na+] - ([Cl-]+[HCO3-]) • 9 ± 3 mEq/L (mmol/L)

  15. Serum AnionGap • Serum AG= Measured - Measured cations anions • Serum AG= Na - (Cl+HCO3) • Serum AG= Unmeasured anions- Unmeasured cations

  16. AnionGap AnionsCations Cl+HCO3 Na Albumin Phosphates K Sulfates Ca Lactates Mg Urates

  17. HIGH SERUM ANION GAP • increase in unmeasured anions metabolic acidosis, hyperalbuminemia, hyperphosphatemia, or overproduction of an anionic paraprotein • reduction in unmeasured cations hypokalemia, hypocalcemia, hypomagnesemia

  18. LOW SERUM ANION GAP  • Decrease in unmeasured anions primarily due to hypoalbuminemia • Increase in unmeasured cations hyperkalemia, hypercalcemia, hypermagnesemia, or severe litium intoxication • Bromide ingestion • serum protein electrophoresis should be obtained to look for a cationic paraprotein that is present in some patients with multiple myeloma

  19. Urinary Anion Gap • UAG=( UNa + UK) – UCl • (-20) — (-50) mEq/L (NH4 +) • The urinary anion gap reflects the ability of the kidney to excrete NH4Cl

  20. SymptomsandSigns • mainly those of the underlying disorder • compensatory hyperventilation is an important clinical sign • Kussmaul breathing (deep, regular, sighing respirations) may be seen with severe metabolic acidosis

  21. LaboratoryFindings • Blood pH, serum HCO3-, and PCO2 are decreased • Anion gap may be normal (hyperchloremic) or increased (normochloremic) • Hyperkalemia may be seen

  22. Treatment: Normal AnionGapAcidosis • Treatment of RTA is mainly achieved by administration of alkali (either as bicarbonate or citrate) to correct metabolic abnormalities and prevent nephrocalcinosis and CKD • Proximal RTA: -large amounts of oral alkali (10–15 mEq/kg/d) -thiazides may reduce the amount of alkali required -mixture of sodium and potassium salts is preferred • Distal RTA: - requiresless alkali(1–3 mEq/kg/d)

  23. Treatment: Normal AnionGapAcidosis • Type IV RTA: -dietary potassium restriction may be necessary and potassium-retaining drugs should be withdrawn -Fludrocortisone may be effective in cases with hypoaldosteronism, but should be used with care, preferably in combination with loop diuretics.

  24. Treatment: IncreasedAnionGapAcidosis • Treatment is aimed at the underlying disorder, such as insulin and fluid therapy for diabetes and appropriate volume resuscitation to restore tissue perfusion • Supplemental HCO3– isindicated for treatment of hyperkalemia • Large amounts of HCO3– may have deleterious effects, including hypernatremia, hyperosmolality, volume overload, and worsening of intracellular acidosis

  25. Treatment: IncreasedAnionGapAcidosis • In salicylate intoxication: -alkali therapy must be started to decrease central nervous system damage unless blood pH is already alkalinized by respiratory alkalosis, since an increased pH converts salicylate to more impermeable salicylic acid • In alcoholic ketoacidosis: -thiamines should be given with glucose to avoid Wernicke encephalopathy • The bicarbonate deficit can be calculated as follows: HCO3=0.5 x b.w. (kg) x (24-HCO3)

  26. Metabolic Alkalosis • Rise in HCO3-concentration with rise in pH • Compensatory response: rise in pH causes decreased respiration, increasing CO2 • raise the PCO2 by 0.7 mmHg for every 1 meq/L elevation in the serum HCO3 concentration

  27. Causes of Metabolic Alkalosis • Loss of Hydrogen 1.Gastroinrestial losses: -gastrik section -vomiting -antacid therapy -chloride-losing diarrhea 2.Renal losses: -diuretics -mineralocorticoid excess -hypercalcemia/milk-alkali syndrom -low chloride intake 3. H+ shift into cell -hypokalemia

  28. Causes of Metabolic Alkalosis 2 • Retention of Bicarbonate -massive blood transfusions -NaHCO3 administration • Contraction alkalosis -diuretics -sweat losses in cystic fibrosis

  29. SymptomsandSigns • Therearenocharacteristicsymptomsorsigns • Orthostatichypotensionmay be encountered • Concomitanthypokalemiamaycauseweaknessandhyporeflexia • Tetanyandneuromuscularirritabilityoccurrarely

  30. LaboratoryFindings • The arterial blood pH and bicarbonate are elevated • Serum potassium and chloride are decreased • The urine chloride can differentiate between saline-responsive (< 25 mEq/L) and unresponsive (> 40 mEq/L) causes

  31. Treatment  • Saline-Responsive Metabolic Alkalosis -correction of the extracellular volume deficit with isotonic saline -H2-blockers or proton pump inhibitors may be helpful in patients with alkalosis from nasogastric suctioning -acetazolamide will increase renal bicarbonate excretion • Saline-Unresponsive Metabolic Alkalosis -surgicalremoval of a mineralocorticoid-producingtumor-blockage of aldosteroneeffectwith an ACE inhibitororwithspironolactone

  32. RespiratoryAcidosis • Rise in CO- concentration with fall in pH • Compensatory response: fall in pH causes increased renal H+ secretion, raising HCO3-concentration • serum HCO3 concentrationincrease by about 1 meq/L for every 10 mmHg elevation in the PCO2

  33. Causes of Respiratory Acidosis • İnhibition of respiratory drive -opiates -anesthetics -sedatives -central sleep apnea -obesity -central nervous system lesions

  34. Causes of Respiratory Acidosis 2 • Disorders of respiratory muscles 1.Muscle weakness; -myastenia gaves -periodic paralysis -aminoglycosides -Guillan-Barre syndrom -spinal cord injury -acute lateral sclerosis -multiple sclerosis 2.Kyphoscoliosis

  35. Causes of Respiratory Acidosis 3 • Upper airway obstruction -obstructive sleep apnea -laryngospasm -aspiration • Lung diseases -pneumonia -severe asthma -pneumothorax -acute respiratory disress syndrom -chronic obsructive pulnmonery disease -interstitial lung disease

  36. Treatment  • Ventilatory support • NaHCO3− therapy controversial in this disorder: -Perhaps beneficial in severely acidemic patient (eg, status asthmaticus) versus -Hazards of therapy in patients with reversible hypercapnea (eg, chronic obstructive pulmonary disease in which respiratory drive is depressed)

  37. RespiratoryAlkalosis • Fall in CO- concentration with rise in pH • Compensatory response: rise in pH causes diminished renal H+ secretion, lowering HCO3-concentration • serum HCO3 concentration fall 2 meq/L for every 10 mmHg decline in the PCO2

  38. Causes of RespiratoryAlkalosis • Hypoxemia 1.Pulmonary disease -pneumonia -interstitial fibrosis -emboli -edema 2.Congestive heart failure 3.Anemia

  39. Causes of Respiratory Alkalosis 2 • Stimulation of the medullary respiratory center -hyperventilation -hepatic failure -septicemia -salycilate intoxication -pregnancy -neurologic disordrs • Mechanical ventilation

  40. Treatment  • Correction of underlying disorder • Increasing Pco2 in inspired air (breathing into paper bag) in setting of acute respiratory alkalosis

  41. Diagnosis of acid-base disorders: a stepwise approach • Step1: Obtain arterial blood gas and electrolyte values simultaneously • Step2: Define the acid-base disorders • Step3: Calculate the anion gap • Step4:Define the limits of compensation to distinguish simple from mixed acid-base disorders • Step5:Make the diagnosis

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