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Acid-Base

Acid-Base. Definitions. Acid: substance that can donate hydrogen ions Base: substance that can accept hydrogen ions. Types of acids. Carbonic acid (volatile acid, carbon dioxide,~ 15000 mmol/d). Eliminated by the lungs

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Acid-Base

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  1. Acid-Base

  2. Definitions • Acid: substance that can donate hydrogen ions • Base: substance that can accept hydrogen ions

  3. Types of acids • Carbonic acid (volatile acid, carbon dioxide,~ 15000 mmol/d). Eliminated by the lungs • Non-carbonic acids (nonvolatile acids such as phosphoric and sulfuric acids, 50 -100 meq/d). Combine with buffers and subsequently excreted by the kidney

  4. Clinical pH range • pH between 7.80 and 6.80 (H+concentrations between 16 -160 neq/l) are the extremes of pH compatible with life • Clinical laboratories measured pH, carbon dioxide, and oxygen in arterial samples • Bicarbonate concentration can be calculated from the Henderson equation • Laboratories measure total CO2 concentration (dissolved CO2 plus bicarbonate concentration, ~25-26 meq/l) in venous samples

  5. Plasma bicarbonate concentration • Laboratories measure total CO2 concentration (dissolved carbon dioxide plus bicarbonate concentration, ~25-26 meq/l) • As a result, total CO2 concentration exceeds plasma bicarbonate concentration by 1.0 to 1.5 meq/l • Normal plasma bicarbonate concentration is approximately 24 mEq/l

  6. Definitions • Reduced pH (elevated hydrogen ion concentration) equals acidemia • Increased pH (reduced hydrogen ion concentration equals alkalemia) • Process that lowers pH = acidosis • Process that increases pH = alkalosis

  7. Bicarbonate buffer system • CO2 + H20  H2CO3  H+ + HCO3- • If a closed system, pKa = 6.1 (normal pH= 7.40) • We are an open system via the lungs excreting CO2 making this system a highly efficient buffer

  8. Determinants of pH • (pH) H+ = 24 ( CO2) (HCO3) • pH must be converted to H+ (nEq/L). pH = 7.40 = 40 nEq/L • 7.40 = 40 = 24 (40/24)

  9. pH 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 [H+] 100 80 64 50 40 32 25 20 16 pH vs. [H+] [H+] = 80 – decimal digits of pH

  10. Normals • Normal pH • 7.35-7.45 (7.40) • pH = -log[H+] • [H+] = 24 x pCO2/[HCO3-] • Normal pCO2 • 36-44 mm Hg (40 mmHg) • Normal HCO3- • 22-26 meq/L (24 meq/l)

  11. Metabolic Disorders • Processes that directly alter bicarbonate concentration Metabolic acidosis: decreased bicarbonate • Metabolic alkalosis: increased bicarbonate

  12. Respiratory Disorders • Processes that directly alter CO2 • Respiratory acidosis: increased CO2 • Respiratory alkalosis: decreased CO2 • Buffer effect: slightly increased HCO3 with respiratory acidosis. Slightly decreased HCO3 with respiratory alkalosis.

  13. Buffering • Prevent wide changes in pH in response to the addition of base or acid • Bicarbonate is the major extracellular buffer (can be easily measured) • There are also intracellular buffers

  14. Effects of Buffers on pH • Bicarbonate is the major extracellular buffer. There are also intracellular buffers. • The presence of buffers attenuates changes in pH in response to acid-base disorders. • Immediate onset • Isohydric principle (all buffers change in the same direction)

  15. Purpose of Acid-Base Balance • Maintain normal pH by buffer systems

  16. Secondary(Compensatory) Mechanisms • In addition to buffering mechanisms, additional secondary (compensatory) physiologic responses occur in response to changes in pH. • Invariably present in simple acid-base disorders (if not present, it is a mixed disorder)

  17. Compensatory mechanisms • The respiratory system compensates for metabolic disorders by altering CO2 (via the lungs, rapid onset, minutes) • Compensation for respiratory disorders occurs by alterations in bicarbonate concentration (via the kidney, slower onset 1-2 days)

  18. Mechanisms that Buffer an Acid Load

  19. Summary

  20. Golden rules: Simple acid-base disorders • 1) PCO2 and HCO3 always change in the same direction. • 2) The secondary physiologic compensatory mechanisms must be present. • 3) The compensatory mechanisms never fully correct pH.

  21. Metabolic acidosis • Process that reduces plasma bicarbonate concentration • Etiology: • Decreased renal acid excretion • Direct bicarbonate losses (GI tract or urine) • Increased acid generation (exogenous or endogenous)

  22. Causes of metabolic acidosis • 1) increased acid generation • Lactic acidosis, Ketoacidosis, ingestion of acids (aspirin, ethylene glycol, methanol), dietary protein intake (animal source) • 2) loss of bicarbonate • Gastrointestinal (diarrhea, intestinal fistulas) • Renal: type 2 proximal renal tubular acidosis

  23. Causes of metabolic acidosis • 1) decreased acid excretion (impaired NH4+ excretion) • Renal failure (reduced GFR) decreased ammonium excretion • Type I (distal) renal tubular acidosis • Type 4 renal tubular acidosis (hypoaldosteronism)

  24. Respiratory acidosis • Induced by hypercapnia (decreased alveolar ventilation) • Buffering mechanisms raise plasma bicarbonate concentration (rapid but limited response, ~1-2 meq/l) • Kidney minimizes the change in extracellular pH by increasing acid excretion (NH4+) generating new bicarbonate ions (delayed response, 2-3 days).

  25. Respiratory alkalosis • Reduced carbon dioxide due to increased alveolar ventilation • Buffering processes lower plasma bicarbonate concentration (rapid but limited response, ~1-2 meq/l) • Kidney response is to reduce net acid excretion (eliminate bicarbonate into the urine or decrease ammonium excretion). Delayed response, 1-2 days)

  26. Respiratory disorders • Acute respiratory acid base disorders always have a greater change in pH than chronic disorders • Plasma Cl changes equally and inversely with plasma HCO3. • Plasma anion gap does not change with respiratory disorders • Plasma sodium is not directly altered by acid base disorders

  27. Metabolic alkalosis • Processes that raise plasma bicarbonate concentration • Etiology: Loss of hydrogen ion from the GI tract (vomiting) or into the urine (diuretic therapy) • Excessive urinary net acid excretion (primary hyperaldosteronism)

  28. Metabolic alkalosis • Urine chloride concentration: • Cl responsive: urine Cl <20 meq/l (usually <10 meq/l • Cl resistant: urine Cl > 20 meq/l (usuallly >50 meq/l)

  29. Expected pH Changes for Respiratory Disorders • Acute Respiratory Acidosis: HCO3- increases 1 mEq for each 10 mm increase in PCO2 • Chronic Respiratory Acidosis: HCO3- increases 4 mEq for each 10 mm increase in PCO2 • Acute Respiratory Alkalosis: HCO3- decreases 2 mEq for each 10 mm decrease in PCO2 • Chronic Respiratory Alkalosis: HCO3- decreases 5 mEq for each 10 mm decrease in PCO2

  30. Plasma anion gap Strong acids (HA) fully dissociate at physiologic pH (7.40) into H+ and A- H+ is buffered by HC03- A- is either excreted into the urine (normal plasma anion gap, increased plasma chloride concentration) Or, A- is reabsorbed by the kidney and retained in plasma, as an unmeasured anion (increased plasma anion gap, minimal change in plasma chloride concentration)

  31. Renal acid excretion • All of the filter of bicarbonate must be reabsorbed (primarily in the proximal tubule and loop of Henle) • Final excretion of the daily acid load occurs primarily in the collecting duct (approximately 50-100 meq/d)

  32. Titratable acidity • Phosphate homeostasis is maintained by urinary excretion of dietary phosphate • Monobasic phosphate is an effective urinary buffer, esp. at lower urinary pH • Accounts for excretion of 10 to 40 mEq of hydrogen ion daily • Cannot be increased beyond this due to the fixed amount of phosphate in urine

  33. Ammonium excretion • Contributes the major adaptive response to an acid load • Can be increased in response to physiologic needs • Normally 30-40 mEq/d and maximal excretion is approximately 300 mEq/d • NH4+ is lipid soluble and therefore trapped in the urinary lumen

  34. Urine anion gap • An indirect estimate of urinary NH4+ excretion • Urine Na + K minus urine Cl • Normally, ~ 10 meq/l • Becomes less positive and may even become neg with incr urinary NH4 excretion (Cl- must accomany NH4+)

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