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Acid Base PowerPoint Presentation

Acid Base

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Acid Base

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    1. Acid & Base John R. Foringer, M.D. Division of Renal Diseases and Hypertension Section of Critical Care Nephrology john.r.foringer@uth.tmc.edu (713) 500-6868

    3. Simple Acid-Base Disturbances pH = pK + log10 [HCO3] (0.0301)(paCO2) pH = 6. 1 + log ( metabolic component) (respiratory component) HCO3_ & CO2 = pH CO2 & HCO3_ = pH

    7. Normal renal processes of acid handling

    12. Mixed Acid-Base Disturbances Definition Combination of two or more of the 4 simple disturbances (primary) Examples Mixed respiratory-metabolic disorders Mixed metabolic disorders

    13. Compensatory Responses in Simple Acid-Base Disorders

    14. What is the Base Excess? Proposed as an indicator of acid-base status that was not influenced by PaCO2 It is the sum of the concentration of buffer anions HCO3 and hemoglobin Problem is this only works in vitro In vivo as the PCO2 rises the ? HCO3 is attenuated by flux into the interstitial fluid compartment Now to overcome this: Standard Base Excess SBE = 0.93 ([HCO3] -24.4) + 13.79 (pH -7.4) Estimates the amount of base needed to restore the metabolic acid-base status to normal in the entire extracellular fluid compartment

    16. Metabolic Acidosis

    17. Why Acidosis is Bad

    19. Evaluating a Low HCO3

    22. Lactic Acid Type I proportional increase in lactate and pyruvate Type II Lactate higher than pyruvate Type A tissue hypoxia Type B arises from malignancy, liver disease, inborn errors of metabolism, or ingestion of toxins

    23. Treatment of Metabolic (Lactic) Acidosis Treatment with NaHCO3 An estimate of replacement Dose of bicarbonate = (0.5 X BW) X (desired HCO3 current HCO3) Goal of replacement is a pH above 7.2

    24. Treatment of Lactic Acidosis Should we treat lactic acid with HCO3 ? ?PFK activity (rate limiting enzyme of glycolysis) Acidosis ?and alkalosis ? lactate production ? CO2 production Impairs cardiac performance Large fluid load

    27. Treatment of Lactic Acidosis Dichloroacetate Promotes oxidation of lactate (pyruvate dehydrogenase) ?? acetyl-coenzyme A + carbon dioxide 252 patients with lactic acidosis, placebo-controlled, randomized trial of intravenous sodium dichloroacetate Only 12 percent of the dichloroacetate-treated patients and 17 percent of the placebo patients survived to be discharged Statistically significant but clinically unimportant changes in arterial-blood lactate concentrations and pH and fails to alter either hemodynamics or survival

    28. THAM (0.3 N tromethamine) Tris-Hydroxymethyl Aminomethane Sodium-free solution Buffers both metabolic acids (THAM + H+ ?? THAM+) and respiratory acids (THAM + H2CO3 ?? THAM+ + HCO3-) [proton and CO2 scavenger] Limits carbon dioxide generation and increases both extracellular and intracellular pH Serious side effects including hyperkalemia, hypoglycemia, ventilatory depression, local injury in cases of extravasation, and hepatic necrosis in neonates Renal excretion

    29. Treatment of Lactic Acidosis Carbicarb Equimolar concentrations of sodium bicarbonate and sodium carbonate Carbonate is a stronger base (CO32- + H+ ?? HCO3-) Carbonate ion can react with carbonic acid, thereby consuming carbon dioxide (CO32- + H2CO3 ?? 2HCO3-). Increased blood and intracellular pH with little or no rise in the arterial or venous partial pressure of carbon dioxide Risks of hypervolemia and hypertonicity

    36. Disorders Responsible for Hyperchloremic Acidosis (Normal Anion Gap) Gastrointestinal Bicarbonate Loss Diarrhea Renal Acidification Defects Proximal, classical distal RTA, and hyperkalemic distal RTA Early chronic renal failure Ingestion or administration of acid, hyperalimentation Drugs

    38. Evaluating a Low Serum HCO3 Renal Tubular Acidosis Impaired ammonium excretion can be demonstrated by the urine net negative charge (anion gap): urine Na + + urine K+ + urine NH4+ = urine Cl- UNa + + UK+ - UCl- = -UNH4+ Normally: UNa + + UK+ - UCl- = -UNH4+ = < -20 in the face of acidemia In RTAs ammonium excretion is impaired, therefore In RTAs: UNa + + UK+ - UCl- = -UNH4+ = 0 ( range +20 to 80)

    40. Normal physiology of acid excretion: Proximal tubule Responsible for reabsorption of the HCO3 filtered at the glomerulus; bulk reabsorption

    44. Metabolic Alkalosis

    45. Metabolic alkalosis Respiratory acidosis Therefore, diagnosis requires a concomitant arterial pH.

    46. Evaluating an Elevated Serum HCO3- Causes of Metabolic Alkalosis Effective ECV Contraction resulting in secondary Hyperreninemic Hyperaldosteronism Hypermineralocorticoidism resulting in ECV expansion and Hypertension. Exogenous Alkali Loads

    51. Treatment of Metabolic Alkalosis Low Urine [Cl-] (< 20 mEq/L) 0.9% NaCl Potassium Chloride High Urine [Cl-] (>25 mEq/L) Cause specific (surgery, angioplasty, specific drug therapy)

    53. Respiratory Acid-Base Disorders Alkalosis Central nervous system lesions, pregnancy, endotoxemia, salicylates, hepatic failure, hypoxemia, anxiety, pain