Acid Base Status in the Intensive Care Unit Edward Omron MD, MPH, FCCP

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A review of acid base disorders in the intensive care unit. A review of strong ion difference and physicochemical analysis in acute illness and major surgery. Clinical applications in electrolyte management,fluid resuscitation, and complex acid-base disorders in critical care medicine

Edward Omron MD, MPH
Pulmonary, Critical Care Medicine
Morgan Hill, CA 95037

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Acid Base Status in the Intensive Care Unit Edward Omron MD, MPH, FCCP

  1. 1. A Primer of Acid-Base Assessment by Physicochemical Analysis and Strong Ion Difference<br />Edward M. Omron MD, MPH, FCCP<br />Pulmonary and Critical Care Medicine<br />edofiron@gmail.com<br />
  2. 2. OBJECTIVES<br />A critical assessment of conventional acid-base analysis<br />A review of strong ion difference and physicochemical analysis in acute illness and major surgery<br />Clinical applications in <br />Electrolyte management<br />Fluid resuscitation<br />Complex acid-base disorders<br />
  3. 3. Metabolic acid-base status<br />What is it?<br />Why is it important?<br />Why assess for it?<br />Can we do better?<br />
  4. 4. A 34-year-old white man presents with nausea, vomiting and has been unable to consume any food or liquids. He admits to drinking about two pints of vodka daily. Temperature is 99.6 F, pulse rate is 101 per minute supine and 126 per minute standing, respirations are 24 per minute, and blood pressure is 110/85 mm Hg supine and 80/50 mm Hg when standing. <br />Which of the following is the most likely explanation for these laboratory findings? <br />(A) Respiratory alkalosis<br />(B) Respiratory alkalosis and metabolic acidosis<br />(C) Metabolic acidosis<br />(D) Respiratory alkalosis, metabolic acidosis, and metabolic alkalosis<br />(E) Metabolic alkalosis, respiratory alkalosis, and respiratory acidosis <br />
  5. 5. Concept of pH<br />pH H+<br /><ul><li>7.0 100 nmol/L
  6. 6. 7.4 40
  7. 7. 7.7 20</li></ul>pH = - log (H+): log linear<br />Exponential in reality<br />
  8. 8. “The duty of the physician is to discover that the quantity of sodium bicarbonate in the blood is diminished, to restore that quantity to normal, and to hold it there. But while restoring it, he must never increase the quantity above normal.”<br />Henderson LJ; Science 1917;46:73-83<br />
  9. 9. Figure 1. Henderson-Hasselbalch Equations<br />H+ + HCO3- H2CO3 CO2 + H2O<br /><ul><li>[H+] = 24 x PCO2/[HCO3-]
  10. 10. pH = 6.1 + Log [HCO3-] / [0.03 x PCO2]</li></ul>pK = 6.1<br />
  11. 11. Slope Intercept H-H Equation<br />y = mx + b<br />Log [PCO2] = -1 (pH) + Log [HCO3-]/K<br />In-vitro log PCO2- pH equilibration curve<br />Linear relationship between log PCO2 and pH<br />Slope = -1<br />
  12. 12. In-Vitro<br />
  13. 13. Gibbs Donnan Effect<br />
  14. 14. Gibbs Donnan Effect<br />Constable P. J Appl Physiol 1997; 83(1): 298<br />
  15. 15. HH Equation<br />Explains the effect of PCO2 on pH<br />PCO2 directly measured<br />Linear relationship between pH and PCO2<br />HH does not explain the effects of:<br />Na+(Hypernatremia, Hyponatremia)<br />Cl- (Hypochloremia, Hyperchloremia)<br />Unmeasured and measured anions and cations<br />lactate, ketones, salicylates, lithium, serum globulins …<br />hypoalbuminemia and hyperphosphatemia<br />Resuscitation Fluids <br />
  16. 16.
  17. 17.
  18. 18. Charge Balance at Standard Physiologic State<br />160<br />K+ Ca++ Mg++<br />140<br />SID = +39<br />120<br />mmol/L<br />100<br />80<br />Cl- = -106<br /> Na+ = 142<br />60<br />40<br />20<br />0<br />Cations<br />Anions<br />
  19. 19. Charge Balance at Standard Physiologic State<br />160<br />K+ Ca++ Mg++<br />140<br /> A- = -14.4<br />SID = +39<br />Buffer Base = -39<br />120<br /> HCO3 = -24.6<br />mEq/L<br />100<br />80<br /> Cl- = -106<br /> Na+ = 142<br />60<br />pH = 7.40<br />PaCO2 = 40 mm Hg<br />BEp = 0 mEq/L<br />SBE = 0 mEq/L<br />ANG = 12 mEq/L<br />SIG = 5 mEq/L<br />40<br />20<br />0<br />Cations<br />Anions<br />
  20. 20. Strong Ions and Charge Balance<br />Na+ + K+ + Mg++ + Ca++ + H+ = Cl- + HCO3- + OH- + lactate- + A- + XA- + Pi-<br />Na+ + K+ + Mg++ + Ca++ -Cl- - lactate- - XA- = HCO3- + A- + Pi-<br />(Na+ + K+ + Mg++ + Ca++ -Cl- - lactate- - XA-) = (HCO3- + A- + Pi-)<br />+39 = ?-39<br />Strong Ion Difference = Buffer Base<br />
  21. 21. Plasma Buffer Base<br />Weak acids: pKa 5.8-8.9<br />Volatile buffer anion bicarbonate<br />HCO3- + H+ = H2CO3 = CO2 + H2O<br />Open buffer system in plasma<br />Nonvolatile Buffer Anions<br />Albumin (imidazole  amino protein groups)<br />Inorganic Phosphorus (PI): H2PO42-<br />Total Citrate <br />J Appl Physiol 1986; 61: 2260-2265<br />
  22. 22.
  23. 23. Standard physiological state in plasma for 70 kg test subject (TBW = 60% total body weight)<br />SID, strong ion difference; Atot, plasma nonvolatile weak acid buffer content; SBE, standard base excess; HCO3, bicarbonate; TBW, total body water; ECV, extracellular compartment volume; PV, plasma volume <br />
  24. 24. Calculation of the SID or Buffer Base<br />Buffer Base  [HCO3-] + 2.8 x [Alb-] g/dL + 0.6 x [Pi] mg/dL<br />BB = -24.6 mEq/L- 2.8 x 4.4 g/dL – 0.6 x (3.6 mg/dL)= -39<br />Figge-Fencl algorithm<br />http://www.figge-fencl.org/<br />
  25. 25. Δ SID Δ buffer base<br />A change in SID forces a change in buffer base<br />Displacement from normal (+39 mEq/L) quantitates metabolic acid-base disorders<br />PCO2 independent index<br />Singer RB, Hastings AB. Medicine 1948; 27: 223-242<br />
  26. 26. Hyperchloremic Metabolic Acidosis<br />160<br />K+ Ca++ Mg++<br />140<br />A- = -13.2<br />Buffer Base = -29<br />SID = +29<br />120<br />HCO3= -15.8<br />mEq/L<br />100<br />80<br />( 10)<br />Cl- = -116<br /> Na+ = 142<br />60<br />pH = 7.209 <br />PCO2 = 40 mm Hg<br />BEp = -10 mE/L<br />SBE = -11 mEq/L<br />ANG = 11 mEq/L<br />SIG = 5 mEq/L<br />40<br />20<br />0<br /> Cations<br />Anions<br />
  27. 27. Buffer Base (BB) in Hyperchloremia<br />BB = -39 mEq/L and Cl- = 106<br />BB = -29 mEq/L and Cl- = 116<br />HCO3- = - 24.6mEq/L<br />HCO3- = -15.8<br />Albumin + PI = -13.2<br />Albumin +PI = -14.4 mEq/L<br />H+ +HCO3- H2CO3 CO2 +H2O<br />BEp = -10 mEq/L<br />
  28. 28. Lactic Acidosis (Lactate- = 10 mmol/L)<br />160<br />K+ Ca++ Mg++<br />140<br /> Alb- + PI= -13.2<br />SID = +29<br />Buffer Base = -29<br />HCO3-= -15.8<br />120<br />Lac- = -10<br />mmol/L<br />100<br />80<br />Cl- = -106<br /> Na+ = 142<br />60<br />40<br />pH = 7.208<br />PCO2 = 40 mm Hg<br />BEp = -10 mmol/L<br />20<br />0<br />Cations<br />Anions<br />
  29. 29. Ketoacidosis (Ketones- = 10 mmol/L)<br />160<br />K+ Ca++ Mg++<br />140<br /> Alb- + PI= -13.2<br />SID = +29<br />Buffer Base = -29<br />HCO3-= -15.8<br />120<br />Ket- = -10<br />mmol/L<br />100<br />80<br />Cl- = -106<br /> Na+ = 142<br />60<br />40<br />pH = 7.208<br />PCO2 = 40 mm Hg<br />BEp = -10 mmol/L<br />20<br />0<br />Cations<br />Anions<br />
  30. 30. Hyperchloremic Phase of DKA<br />160<br />K+ Ca++ Mg++<br />140<br /> Alb- + PI= -13.2<br />SID = +29<br />Buffer Base = -29<br />120<br />HCO3-= -15.8<br />mmol/L<br />100<br />80<br />( 10)<br />Cl- = -116<br /> Na+ = 142<br />60<br />40<br />pH = 7.208 <br />PCO2 = 40 mm Hg<br />BEp = -10 mmol/L<br />20<br />0<br /> Cations<br />Anions<br />
  31. 31. Hypochloremic Metabolic Alkalosis<br />160<br />K+ Ca++ Mg++<br />140<br /> A- = -15.2<br />Buffer Base = - 49<br />SID = +49<br />120<br />HCO3= -33.8<br />100<br />mEq/L<br />80<br />( 10)<br />Cl- = -96<br /> Na+ = 142<br />60<br />pH = 7.54<br />PCO2 = 40 mm Hg<br />BEp = 10 mEq/L<br />SBE = 11 mEq/L<br />ANG = 13<br />40<br />20<br />0<br /> Cations<br />Anions<br />
  32. 32. pH as a function of SID<br />-<br />+<br />
  33. 33. Etiology of Metabolic Acid-Base Disturbances<br />Changes in Strong Ion Difference<br />Increased = Metabolic Alkalosis<br />Excess of plasma cations<br />Reduced = Metabolic Acidosis<br />Excess of plasma anions<br />*Summarizes Acid-Base Status Circa 1962<br />
  34. 34. 24 29 34 39 44 49 54<br />SID (mEq/L)<br />*Summarizes Acid-Base Status Circa 1962<br />
  35. 35. BE Scale for Metabolic Acid-Base Disorders<br />Excess Anions < -2 mMol/L (Metabolic Acidosis)<br />Excess Cations > +2 mMol/L (Metabolic Alkalosis)<br />Change from 39 reflects of degree of anion / cation disparity only regarding strong ions<br />Magnitude of metabolic component of acid-base status in plasma compartment<br />Not Standard Base Excess (SBE)<br />PCO2 independent index<br />*Siggard-Anderson O. Scand J Clin Lab Invest 1962; 14: 598-604<br />
  36. 36. Standard Base Excess<br /><ul><li>{+} value</li></ul> excess plasma cations = metabolic alkalosis<br /><ul><li>{-} value</li></ul> excess plasma anions = metabolic acidosis<br /><ul><li>Magnitude of metabolic component of acid-base status in extracellular fluid compartment</li></ul>Adjusts for Gibbs Donnan effect unlike BEp<br /><ul><li>Metabolic Acidosis </li></ul>PCO2 = SBE then normal compensation<br /><ul><li>Respiratory acidosis/alkalosis (pure)</li></ul>SBE = 0<br />PCO2 independent index<br />
  37. 37. Which profile has the most severe metabolic acid-base derangement?<br />A. pH = 7.19, PCO2 = 40, HCO3 = 15<br />B. pH = 7.55, PCO2 = 18, HCO3 = 15<br />C. pH = 7.10, PCO2 = 74, HCO3 = 22<br />
  38. 38. Which profile has the most severe metabolic acid-base derangement?<br />A. pH = 7.19, PCO2 = 40, HCO3 = 15<br />SBE = -11.6 mmol/L<br />B. pH = 7.55, PCO2 = 18, HCO3 = 15<br />SBE = -6.6 mmol/L<br />C. pH = 7.10, PCO2 = 74, HCO3 = 22<br />SBE = -6.4 mmol/L<br />
  39. 39. Dehydration <br />Dehydration and Water intoxication<br />Water loss/gain from intracellular and interstitial compartments<br />Associated with hypertonicity/hypotonicity and changes in plasma [Na+] (excludes uremia, DKA, NKHC, mannitol…)<br />Symptoms: thirst, confusion, coma<br />Quantitatively described as free water deficiency /excess<br />Volume of water that must be removed/added to hypotonic/hypertonic plasma to make isotonic plasma<br />Treatment: D5W with electrolytes, diuretics, and hypertonic saline<br />Language Guiding Therapy: The Case of Dehydration versus Volume Depletion<br />Ann Intern Med 1997;127:848-853<br />
  40. 40. Volume Depletion<br />Volume depletion/expansion (hypo and hypervolemia)<br />Extracellular fluid compartment volume depletion/excess that affects the vascular tree<br />Surrogate term for where cardiac function lies on the Starling Curve<br />Diagnosis: <br />Macrocirculation Impairment: BP, HR, Orthostatics<br />Microcirculation Impairment: Lactic Acidosis, Low venous Svo2<br />Treatment: Crystalloids, Colloids, PRBC, or diuretics<br />
  41. 41. Dehydration versus Volume Depletion<br />Changes in extracellular and intracellular compartment volumes can be and often are dissociated<br />Indiscriminate use of the terms dehydration and volume depletion risks confusion and therapeutic errors<br />
  42. 42. Treatment of Dehydration Versus Hypovolemia<br />Language Guiding Therapy: The Case of Dehydration versus Volume Depletion<br />Ann Intern Med 1997;127:848-853<br />
  43. 43. Free Water Excess/Deficit effects on [Cl-]<br />Free H2O abnormality detected as an abnormal [Na+]<br />Plasma [Cl-] has to be corrected for the dilution or concentration of plasma [Na+]<br />[Cl-] predicted = [Cl-] normal x [Na+] observed / [Na+] normal<br />If plasma [Na+] =155 mmol/L <br />Then [Cl-] = 106 x 155/142 = 115 mmol/L<br />If plasma [Na+] =131 mmol/L <br />Then [Cl-] = 106 x 131/142 = 97 mmol/L<br />
  44. 44. Free H2O excess/deficit effects on Plasma [Na+]<br /> Free H2O [Na+] [Cl-]  SID/SID<br />Concentrational <br />Alkalosis<br />Standard State<br />Dilutional Acidosis<br />Nguyen M. and Kurtz I: J Applied Physiology 2006; 100: 1293–1300 <br />
  45. 45. A 34-year-old white man presents with nausea, vomiting and has been unable to consume any food or liquids. He admits to drinking about two pints of vodka daily. Temperature is 99.6 F, pulse rate is 101 per minute supine and 126 per minute standing, respirations are 24 per minute, and blood pressure is 110/85 mm Hg supine and 80/50 mm Hg when standing. <br />Cl-(corrected) =106 x 134/142<br />=100 mEq/L<br />Cl-(observed) = 83 mEq/L<br />17 mEq/L excess cations<br />BEp = +17 strong cations<br />ANGcorr = 33 or -17 anions <br />Which of the following is the most likely explanation for these laboratory findings? <br />(A) Respiratory alkalosis<br />(B) Respiratory alkalosis and metabolic acidosis<br />(C) Metabolic acidosis<br />(D) Respiratory alkalosis, metabolic acidosis, and metabolic alkalosis<br />(E) Metabolic alkalosis, respiratory alkalosis, and respiratory acidosis <br />
  46. 46. Etiology of Metabolic Acid-Base Disturbances<br />Changes in Strong Ion Difference<br />Increased = Metabolic Alkalosis<br />Excess of plasma cations<br />Reduced = Metabolic Acidosis<br />Excess of plasma anions<br />Water deficit/excess:<br />Hypernatremia = Alkalosis (Cation Excess)<br />Hyponatremia = Acidosis (Cation Deficient)<br />Cation/Anion Imbalance<br />Hypochloremia = alkalosis (Anion Deficient)<br />Hyperchloremia = acidosis (Anion Excess)<br />Organic Acids (lactate, Ketones…) = acidosis<br />Anion Excess<br />*Summarizes Acid-Base Status Circa 1962<br />
  47. 47. Standard Physiologic State [Pi] = 3.6 mg/dL<br />160<br />K+ Ca++ Mg++<br />140<br /> Alb- + PI= -14.4<br />SID = +39<br />Buffer Base = -39<br />120<br />HCO3-= -24.6<br />mmol/L<br />100<br />80<br />Cl- = -106<br /> Na+ = 142<br />60<br />40<br />pH = 7.40<br />PCO2 = 40 mm Hg<br />BEp = 0 mEq/L<br />20<br />0<br />Cations<br />Anions<br />
  48. 48. Hyperphosphatemic Metabolic Acidosis [Pi] = 10 mg/dL<br />160<br />K+ Ca++ Mg++<br />140<br /> Alb- + PI= -17.8<br />SID = +39<br />Buffer Base = -39<br />120<br />HCO3-= -21.2<br />mmol/L<br />100<br />80<br />Cl- = -106<br /> Na+ = 142<br />60<br />40<br />pH = 7.337<br />PCO2 = 40 mm Hg<br />BEp = -3.7 mEq/L<br />20<br />0<br />Cations<br />Anions<br />
  49. 49. Standard State Acid Base Status<br />[Alb-] = 0 mg/dL<br />160<br />K+ Ca++ Mg++<br />140<br /> A-= - 2.7<br />SID = +39<br />Buffer Base = -39<br />120<br />HCO3-= - 36.3<br />mEq/L<br />100<br />80<br /> Cl- = -106<br /> Na+ = 142<br />60<br />pH = 7.571<br />PCO2 = 40 mm Hg<br />BEp = 13 mEq/L<br />SBE = 13 mEq/L <br />ANG = 1<br />40<br />20<br />0<br />Cations<br />Anions<br />
  50. 50. Fencl V, Rossing TH. Ann Rev Med 1989; 40:17-29<br />
  51. 51. Hyperchloremic Acidosis [Alb-] = 4.4 gm/dL<br />160<br />K+ Ca++ Mg++<br />140<br /> Alb- + PI= - 13.2<br />SID = +29<br />Buffer Base = -29<br />120<br />HCO3-= - 15.8<br />mmol/L<br />100<br />80<br />( 10)<br />Cl- = -115<br /> Na+ = 142<br />60<br />40<br />pH = 7.208 <br />PCO2 = 40 mm Hg<br />BEp = -10 mEq/L<br />20<br />0<br /> Cations<br />Anions<br />
  52. 52. Hyperchloremic strong ion acidosis with concurrent hypoalbuminemic alkalosis ([albumin] = 2g/dL) <br />160<br />A- = - 7.8<br />K+ Ca++ Mg++<br />140<br />Buffer Base = -29<br />SID = +29<br />HCO3= - 21.2<br />120<br />100<br />mEq/L<br />80<br />( 10)<br />Cl- = -116<br /> Na+ = 142<br />60<br />pH = 7.338<br />PCO2 = 40 mm Hg<br />SBE = - 4 mEq/L<br />ANG = 6 mEq/L<br />Adj. ANG = 12 mEq/L<br />SIG = 5 mEq/L<br />40<br />20<br />0<br /> Cations<br />Anions<br />
  53. 53. Hypoalbuminemic Alkalosis<br />BB = -29<br />BB = -29<br /> HCO3- = -21.2 mEq/L<br /> HCO3- = -15.8mEq/L<br />Albumin<br /> 4.4 g/dL<br />Charge = -13.2 mEq/L<br />Charge =<br />-7.8 mEq/L<br />Albumin<br />2.0 g/dL<br />H+ +HCO3- H2CO3 CO2 +H2O<br />
  54. 54. Hypoalbuminemia- an adaptive response<br />Hypoalbuminemia independent risk factor<br />Beneficial by restoring pH towards normal<br />SBE = -10 mmol/L(Lactate = 10 mmol/L)<br /><ul><li>[Albumin-] = 4.4 g/dL, pH = 7.20
  55. 55. 2.2 g/dL, pH = 7.33
  56. 56. 1.1 g/dL, pH = 7.38</li></ul>J Appl Physiol 1986; 61: 2260-2265<br />
  57. 57.
  58. 58. J Appl Physiol 1986; 61: 2260-2265<br />
  59. 59. Hypoalbuminemia pervasive in acute illness and surgery<br />Hypoalbuminemic alkalosis exists to some extent in all critically ill patients<br />Hypoalbuminemia corrects pH towards standard state in acute illness<br />Am J Respir Crit Care Med 2000; 162: 2246-2251<br />
  60. 60. Etiology of Metabolic Acid-Base Disturbances<br />Changes in Strong Ion Difference<br />Increased = Metabolic Alkalosis<br />Excess of plasma cations<br />Reduced = Metabolic Acidosis<br />Excess of plasma anions<br />Water deficit/excess:<br />Hypernatremia = Alkalosis (Cation Excess)<br />Hyponatremia = Acidosis (Cation Deficient)<br />Cation/Anion Imbalance<br />Hypochloremia = alkalosis (Anion Deficient)<br />Hyperchloremia = acidosis (Anion Excess)<br />Organic Acids (lactate, Ketones…) = acidosis<br />Anion Excess<br />Abnormal concentrations of plasma weak acids<br />Independent determinants of pH<br />Hypoalbuminemia = metabolic alkalosis<br />Hyperalbuminemia = metabolic acidosis<br />Hyperphosphatemia = metabolic acidosis<br />*Summarizes Acid-Base Status Circa 1982<br />
  61. 61. Am J Respir Crit Care Med Vol 162. pp 2246–2251, 2000<br />
  62. 62. Anion Gap (1977)<br />Law of electrical neutrality<br />Discrepancy between cations and anions virtual<br />Na+ + K+ = Cl- + HCO3- + XA-<br />(Na+ + K+ - Cl- - HCO3)  16<br />Facilitates differential diagnosis (easy to compute)<br />Normal ANG entirely accounted for by [albumin] + PI<br />ANG = 2.8*Albumin + 0.5 *PI<br />Very Unreliable in critical illness<br />Hypoalbuminemia<br />pH changes<br />Gibbs Donnan Effect<br />Oh MS & Carroll HJ. The Anion Gap. NEJM 1977; 297: 814-817.<br />
  63. 63. Anion Gap<br />XA-= Unmeasured Anions:<br /> Cyanide<br /> Glycols<br /> Iron<br /> Isoniazid<br /> Ketoacids<br /> Krebs Cycle<br /> Lactate<br /> Methanol<br /> Paraldehyde<br /> Toluene <br /> Salicylate<br /> Uremia<br />160<br />XA-<br />K+ = 4<br />140<br />ANG<br />A- = -14.4<br />120<br />HCO3= -24.6<br />100<br />mEq/L<br />80<br />Na+= 142<br />Cl- = -105<br />60<br />pH = 7.40<br />PCO2 = 40 mm Hg<br />SBE = 0 mEq/L<br />ANG = 12 mEq/L<br />SIG = 5 mEq/L<br />40<br />20<br />0<br />Cations<br />Anions<br />
  64. 64. 68 yo male UGI Bleed<br />Na =132, K = 4, Cl = 98, HCO3 = 22<br />Lactate = 4.5, Alb = 2.8<br />ANG = Na + K – Cl – HCO3 = 16 (“normal”)<br />ANG(c) = 16 + 2.8(4.4 - 2.8) = 20.5 (abnormal)<br />WHY? <br />Adding back lost charge from hypoalbuminemia<br />Anion gap and hypoalbuminemia. Crit Care Med. 1998 Nov;26(11):1807–1810 <br />
  65. 65. Anion Gap = ( Na+ + K+ – Cl- – HCO3-)<br />Fencl V, Rossing TH. Ann Rev Med 1989; 40:17-29<br />
  66. 66. Anion Gap = ( Na+ + K+ – Cl- – HCO3-)<br />
  67. 67.
  68. 68. Strong Ion Gap<br />Unmeasured Anions of Critical Illness<br />All organic anions (ketones, lactate …)<br />Codeterminants of Strong Ion Difference<br />SIG = SID(apparent) – Buffer Base<br />SIDa = Na+ + K+ +Ca+++ Mg++ - Cl- - Lactate-<br />Not affected by pH or [Albumin]<br />Equivalent to the Anion Gap (corrected)<br />
  69. 69. Strong Ion Gap: SIDa – BB = SIG<br />SIDa = Na+ + K+ + Ca2+ + Mg2+ - Cl- - lactate- - XA-<br />Strong Ion Gap<br /> K+ Ca2+ Mg2+<br />XA-<br />140<br /> Alb- + PI= -14.4<br />SIDa<br />120<br />Buffer Base<br />HCO3-= -24.6<br />mmol/L<br />100<br />Lactate-<br />80<br /> Na+ = 142<br />Cl- = -106<br />60<br />40<br />pH = 7.40<br />PCO2 = 40 mm Hg<br />BEp = 0 mmol/L<br />20<br />0<br />Cations<br />Anions<br />
  70. 70. Strong Ion Gap<br />160<br />XA-<br />Strong Ion Gap<br />K+ = 4<br />140<br />A- <br />SIDa<br />120<br />SIDe or Buffer Base<br />HCO3<br />100<br />mEq/L<br />80<br />Na+= 142<br />Cl- = -106<br />60<br />pH = 7.40<br />PCO2 = 40 mm Hg<br />SBE = 0 mEq/L<br />ANG = 12 mEq/L<br />SIG = 5 mEq/L<br />40<br />20<br />0<br />Cations<br />Anions<br />
  71. 71.
  72. 72. Calculation of the SID and apparent SID<br />Buffer Base  [HCO3-] + 2.8 x [Alb-] g/dL + 0.6 x [Pi] mg/dL<br />BB = -24.6 mEq/L- 2.8 x 4.4 g/dL – 0.6 x (3.6 mg/dL)= -39<br />SIDa  Na+ + K+ + (Mg2+ + Ca 2+) - Cl- - lactate-<br />SIDa  Na+ + K+ + 3 – Cl- - lactate- = 42 mEq/L<br />SIG = SIDa – Buffer Base<br />SIG = 42 – 39  3 mEq/L <br />
  73. 73. Independent Determinants of pH<br />Strong Ion Difference (SID)<br />Strong Ion Gap<br />Plasma Weak Acids <br />CO2 production<br />This is physico-chemical analysis!<br />
  74. 74. Physico-Chemical Analysis<br />Three independent determinants of acid-base status<br />Strong Ion Difference <br />PCO2<br />Variable weak acid total ([albumin-] + PI)<br />Mechanistic and quantitative<br />Guides diagnosis and therapy<br />Stewart P. Can J. Physiol. Pharmacology 1983; 61: 1444-1461<br />
  75. 75. Isotonic Crystalloid Solutions<br />-1.8 SBE/L +0.4 SBE/L +4 SBE/L +9 SBE/L<br />*Caution must be exercised in patients with acute or chronic renal failure<br /> and K containing solutions (LR)<br />*NaHCO3 solution: 3 Amps NaHCO3 in 1 Liter sterile water or D5W<br />
  76. 76. Crystalloid SID and serum [HCO3-]<br />If crystalloid SID  plasma [HCO3-] (24.6 mmol/L)<br />No change in SBE or acid-base status<br />Lactated Ringer’s, Hartman’s Solution, Hextend<br />If crystalloid SID < plasma [HCO3-]<br />Metabolic acidosis<br />Normal Saline<br />If crystalloid SID > plasma [HCO3-]<br />Metabolic alkalosis<br />Plasmalyte, ½ NS + 75 mEq/L NaHCO3, and isotonic bicarbonate solutions<br />Omron E: J Int Care Med 2010. 25; 271-280<br />
  77. 77. Metabolic Acid-Base Effects of Crystalloid Infusion<br />Omron E: J Int Care Med 2010. 25; 271-280<br />
  78. 78. Physicochemical Resuscitation<br />Principles<br />Patients in shock with a metabolic acidosis are optimally managed with isotonic crystalloid solutions that are alkaline when infused<br />Patients with normal acid base status are best managed with isotonic balanced solutions<br />Patients with metabolic alkalosis are optimally managed with isotonic solutions that are acidic when infused <br />The principles of Early Goal Directed Therapy are to be done concurrently with physicochemical resuscitation<br />
  79. 79. Dialysis<br />4<br />4<br />1**<br />1<br />0**<br />3<br />2<br />0**<br />0**<br />0 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid<br />1 = Normal Saline (SID = 0), 1.8 mmol/L acid<br />2 = Lactated Ringers ( SID = 28), 0.4 mmol/L base<br />3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base<br />4 = 3 Amps NaHCO3 in sterile H20 in 1 liter (SID = +150), 9 mmol/L base Edward Omron MD, MPH<br />** Acetazolamide 250 mg IVP q12, no more than 500 mg qday Pulmonary / Critical Care<br />
  80. 80. Isotonic (Normal) Saline<br />0.9% Sodium Chloride in sterile water<br />Na+ = 154 mmol/L, Cl- = 154 mmol/L<br />SID = 0<br />Excellent choice in<br />Hypovolemic, Hypochloremia with metabolic alkalosis<br />SBE ≥ 0<br />1.8 mmol/L fixed acid generated (excess Cl-)<br />-1.8 SBE/Liter infused<br />
  81. 81. Lactated Ringer’s Solution<br />Polyionic isotonic crystalloid that mimics plasma electrolyte concentration<br />Na+ = 130, K+=4, Cl- = 109, Lact- = 28, Ca++ = 3<br />SID = 28<br />Excellent choice in mild metabolic acidosis with preserved renal function(SBE = -5 to +5)<br />0.4 mmol/L fixed base<br />0.4 SBE/Liter infused<br />
  82. 82. 1/2 NS with 75 mEq/L HCO3<br />1/2 NS + 1.5 Amps Na HCO3 per liter<br />Isotonic resuscitation and maintenance<br />Na+ =150 mmol/L, Cl- = 75 mmol/L HCO3 = 75 mmol/L<br />SID = +75<br />Hyperchloremic metabolic acidosis and reduced renal function Plasma SBE -10 to -5<br />4 mmol fixed base/Liter infused<br />+4 SBE/ Liter<br />
  83. 83. Isotonic NaHCO3- Administration<br />3 Amps Na HCO3 in 1 liter sterile H2O<br />Isotonic Resuscitation and maintenance<br />Na+ = 150, HCO3 = 150<br />SID = 150<br />Excellent choice in malignant acidemias<br />Bridge to acute dialysis: SBE ≤ -10<br />+9 mmol fixed base/ Liter infused<br />+9 SBE/Liter<br />
  84. 84. Metabolic Acid-Base Effects of Crystalloid Infusion during moderate metabolic acidosis<br />Omron E: J Int Care Med 2010. 25; 271-280<br />
  85. 85. Assumptions<br />Normal renal function<br />Acute and chronic kidney injury result in marked impairment in chloride excretion<br />VD may change in acute illness and surgery<br />Ignores the effects of tissue buffering<br />
  86. 86. Bicarbonate Solutions<br />Historically: hyperosmolar solution<br />1 amp = 50 mEq/50 cc or 1 mEq/cc (1 M)<br />Correction of extracellular acidosis at the expense of massive intracellular derangement<br />No defined physico-chemical endpoint<br />Hypertonic volume expansion<br />Recently shown to increase mortality in shock<br />Only use isotonic solutions: Sterile water or D5W + 3 amps Na HCO3! (0.15 M)<br />Activates Phosphofructokinase !<br />Aggravates minute ventilation !<br />
  87. 87. Alkalosis activates PFK<br />**Aggravates lactic acidosis in shock states<br />
  88. 88. 28 yo male with ARDS undergoing diuresis<br />pH = 7.61, PaCO2 = 40 mm Hg, <br />[HCO3-]HH = 39.4 mmol/L, <br />SBE = 16.8 mmol/L<br />Na+ = 144 mmol/L, Cl- = 91 mmol/L<br />Cl- corrected = 106 x 144/142 = 107<br />Cl- loss 16 mmol/L ( 107-91) = 16 mmol/L excess cations<br />Severe hypochloremic metabolic alkalosis<br />Mechanism?<br />Treatment?<br />
  89. 89. Dialysis<br />4<br />4<br />1**<br />1<br />0**<br />3<br />2<br />0**<br />0**<br />0 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid<br />1 = Normal Saline (SID = 0), 1.8 mmol/L acid<br />2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base<br />3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base<br />4 = 3 Amps NaHCO3 in sterile H20 in 1 liter (SID = +150), 9 mmol/L base Edward Omron MD, MPH<br />** Acetazolamide 250 mg IVP q12, no more than 500 mg qd Pulmonary / Critical Care<br />
  90. 90. 67 yo female with ischemic bowel<br />BP 80/40, HR 120, HCT= 25<br />pH = 7.26, PaCO2 = 24, HCO3 = 11, <br />SBE = -14.6<br />Na+ = 143, Cl- = 118<br />Cl- corrected = 106 x 143/142  106 <br />Excess Cl- (118 - 106) = 12 mmol/L<br />Mechanism: Hyperchloremia<br />How do you fix?<br />What are the resuscitation fluids of choice?<br />
  91. 91. Dialysis<br />4<br />4<br />1**<br />1<br />0**<br />3<br />2<br />0**<br />0**<br />0 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid<br />1 = Normal Saline (SID = 0), 1.8 mmol/L acid<br />2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base<br />3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base<br />4 = 3 Amps NaHCO3 in sterile H20 in 1 liter (SID = +150), 9 mmol/L base Edward Omron MD, MPH<br />** Acetazolamide 250 mg IVP q12, no more than 500 mg qd Pulmonary / Critical Care<br />
  92. 92. 78 yo with severe pneumonia and sepsis<br />pH=7.37, PCO2=26.9, HCO3=15.2, <br />SBE = -9, <br />Na = 134 and Cl = 113 and albumin = 3 g/dL<br />Cl- corrected = 106 x 134/142 = 100 mmol/L<br />Excess chloride = 13 mmol/L<br />Mechanism of metabolic acidosis<br />Hyperchloremia<br />Free water excess reducing Na<br />Hypoalbuminemic Alkalosis<br />How do you fix? <br />Resuscitation Fluid?<br />
  93. 93. Dialysis<br />4<br />4<br />1**<br />1<br />0**<br />3<br />2<br />0**<br />0**<br />0 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid<br />1 = Normal Saline (SID = 0), 1.8 mmol/L acid<br />2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base<br />3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base<br />4 = 3 Amps NaHCO3 in sterile H20 in 1 liter (SID = +150), 9 mmol/L base Edward Omron MD, MPH<br />** Acetazolamide 250 mg IVP q12, no more than 500 mg qd Pulmonary / Critical Care<br />
  94. 94. Additional References<br />http://www.slideshare.net/edofiron<br />www.acidbase.org<br />http://www.figge-fencl.org/<br />Intensive Care Medicine 2011. 37; 461-468.<br />J. Intensive Care Medicine 2010. 25; 271-280.<br />Intensive Care Medicine 2009. 35; 1377-1382.<br />Critical Care Medicine 2005. 21; 329-346.<br />Best Practice Res Clin Anes 2004. 18; 113-127.<br />Kidney Inter. 2003. 64; 777-787.<br />Am. J. Respir. Crit. Care Med. 2000. 162; 2246-2251.<br />J. Applied Physiology 1999. 86; 326-334.<br />Annual Review Medicine 1989. 40; 17-29.<br />

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