Your SlideShare is downloading. ×
Acid Base Disorders in Critical Care Medicine   Edward Omron MD, MPH
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×

Introducing the official SlideShare app

Stunning, full-screen experience for iPhone and Android

Text the download link to your phone

Standard text messaging rates apply

Acid Base Disorders in Critical Care Medicine Edward Omron MD, MPH

1,673
views

Published on

A comprehensive initial evaluation of acid-base disorders in critical care medicine by strong ion difference and physicochemical analysis for housestaff rotating through the ICU …

A comprehensive initial evaluation of acid-base disorders in critical care medicine by strong ion difference and physicochemical analysis for housestaff rotating through the ICU
Edward Omron MD, MPH, FCCP


2 Comments
9 Likes
Statistics
Notes
No Downloads
Views
Total Views
1,673
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
136
Comments
2
Likes
9
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide
  • Notice how the pH is bouyed upso to speak. This is a remarkable adaptive buffering process in acute illness/surgery which escaped the attention of the acid-base physiologists. In fact: all acid base research up to the mid 1980 ’s assumed albumin and phosphate were fixed quantities and did not change in critical illness BIG MISTAKE!!!!!
  • Transcript

    • 1. Acid Base Disorders in the IntensiveCare Unit for HousestaffEdward M. Omron MD, MPH, FCCPPulmonary and Critical Care MedicineMorgan Hill, CA 95037www.docomron.comedofiron@gmail.com
    • 2. OBJECTIVES• A critical assessment of conventional acid-base analysis• A review of strong ion difference andphysicochemical analysis in acute illnessand major surgery– Clinical applications in• Electrolyte management• Fluid resuscitation• Complex acid-base disorders
    • 3. • Metabolic acid-base status–What is it?–Why is it important?–Why assess for it?–Can we do better?
    • 4. A 34-year-old white man presents with nausea, vomiting and has beenunable to consume any food or liquids. He admits to drinking about two pintsof vodka daily. Temperature is 99.6 F, pulse rate is 101 per minute supine and126 per minute standing, respirations are 24 per minute, and blood pressureis 110/85 mm Hg supine and 80/50 mm Hg when standing.Sodium 134 mEq/LPotassium 3.8 mEq/LChloride 83 mEq/LBicarbonate 24 mEq/LPO2 89 mm HgPCO2 32 mm HgpH 7.48Which of the following is the most likely explanation for these laboratoryfindings?(A) Respiratory alkalosis(B) Respiratory alkalosis and metabolic acidosis(C) Metabolic acidosis(D) Respiratory alkalosis, metabolic acidosis, and metabolic alkalosis(E) Metabolic alkalosis, respiratory alkalosis, and respiratory acidosis
    • 5. • Concept of pH– pH H+7.0 100 nmol/L7.4 407.7 20– pH = - log (H+): log linear– Exponential in reality
    • 6. “The duty of the physician is to discover thatthe quantity of sodium bicarbonate in theblood is diminished, to restore that quantityto normal, and to hold it there. But whilerestoring it, he must never increase thequantity above normal.”Henderson LJ; Science 1917;46:73-83
    • 7. Figure 1. Henderson-Hasselbalch EquationsH+ + HCO3- H2CO3 CO2 + H2O[H+] = 24 x PCO2/[HCO3-]pH = 6.1 + Log [HCO3-] / [0.03 x PCO2]pK = 6.1
    • 8. Slope Intercept H-H Equation• y = mx + b• Log [PCO2] = -1 (pH) + Log [HCO3-]/K• In-vitro log PCO2- pH equilibration curve– Linear relationship between log PCO2 andpH– Slope = -1
    • 9. Log PCOLog PCO22--pH Curve in PlasmapH Curve in PlasmapHLogPCO2KPConstable,P. J. Appl. Physiol. 1997; 83(1): 2986.8 7.0 7.2 7.4 7.6 7.8 8.0 8.21.01.21.41.61.82.0In-Vitro
    • 10. Log PCOLog PCO22--pH Curve in PlasmapH Curve in PlasmapHLogpCO2,kPascal6.8 7.0 7.2 7.4 7.6 7.8 8.0 8.21.01.21.41.61.82.0 Blue : in vitroGreen: in vivoCrit Care Med 1998;26:1173-1179Gibbs Donnan Effect
    • 11. Log PCOLog PCO22--pH Curve in PlasmapH Curve in PlasmapHLogPCO2,kP6.8 7.0 7.2 7.4 7.6 7.8 8.0 8.21.01.21.41.61.82.0[Na+][Cl-]Blue : in vitroGreen: in vivoRed: Total ProteinConstable P. J Appl Physiol 1997; 83(1): 298Gibbs Donnan Effect
    • 12. HH Equation• Explains the effect of PCO2 on pH– PCO2 directly measured– Linear relationship between pH and PCO2• HH does not explain the effects of:– Na+ (Hypernatremia, Hyponatremia)– Cl- (Hypochloremia, Hyperchloremia)– Unmeasured and measured anions and cations• lactate, ketones, salicylates, lithium, serum globulins …– hypoalbuminemia and hyperphosphatemia– Resuscitation Fluids
    • 13. Law of Electrical NeutralityLaw of Electrical NeutralityCationsCations == AnionsAnions
    • 14. Plasma Strong IonsPlasma Strong Ions• Strong cations and anions– Na+, K+, Ca++, Mg++, Cl-, Lactate-– Fully dissociated, exert no buffering effect– Combined positive electrical effect• Strong Ion Difference (SID)– Collective unit of charge (mEq/L)– Strong cations - anions• Na++K++Ca+++Mg++-Cl- - lactate = +39 mEq/L– Approximated by difference between Na+ and Cl-
    • 15. 20406080100120140160mmol/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -1060SID = +39Charge Balance at Standard Physiologic State
    • 16. 20406080100120140160mEq/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -106HCO3 = -24.6A- = -14.40Buffer Base = -39SID = +39pH = 7.40PaCO2 = 40 mm HgBEp = 0 mEq/LSBE = 0 mEq/LANG = 12 mEq/LSIG = 5 mEq/LCharge Balance at Standard Physiologic State
    • 17. Strong Ions and Charge BalanceNa+ + K+ + Mg++ + Ca++ + H+ = Cl- + HCO3- + OH- + lactate- + A- + XA- + Pi-Na+ + K+ + Mg++ + Ca++ - Cl- - lactate- - XA- = HCO3- + A- + Pi-(Na+ + K+ + Mg++ + Ca++ - Cl- - lactate- - XA-) = (HCO3- + A- + Pi-)+39 = ?-39Strong Ion Difference = Buffer Base
    • 18. Plasma Buffer Base• Weak acids: pKa 5.8-8.9• Volatile buffer anion bicarbonate– HCO3- + H+ = H2CO3 = CO2 + H2O– Open buffer system in plasma• Nonvolatile Buffer Anions– Albumin (imidazole  amino protein groups)– Inorganic Phosphorus (PI): H2PO42-– Total CitrateJ Appl Physiol 1986; 61: 2260-2265
    • 19. Plasma Buffer Base (BB)Plasma Buffer Base (BB)• Total buffer capacity of plasma– [HCO3-] - 24.6 mEq/L– [Alb] + [PI] +[Citrate] - 14.4 mEq/LNORMAL = - 39 mEq/Lhttp;/www.Figge-Fencl.org/
    • 20. Standard physiological state in plasma for 70 kg testsubject (TBW = 60% total body weight)SID, strong ion difference; Atot, plasma nonvolatile weak acid buffer content; SBE, standardbase excess; HCO3, bicarbonate; TBW, total body water; ECV, extracellular compartmentvolume; PV, plasma volumepH RegulatingVariablesDerivedParametersSID (mEq/L) 39 Weight (Kg) 70.0 pH 7.400PCO2 (mm Hg) 40.0 TBW (L) 42.0 [HCO3]HH (mEq/L) 24.6Atot ECV (L) 14.0 SBE (mEq/L) 0.2Albumin (g/dL) 4.40 PV (L) 3.5Phosphate (mmol/L) 1.16Citrate total (mmol/L) 0.135
    • 21. Calculation of the SID or Buffer Base• Buffer Base  [HCO3-] + 2.8 x [Alb-] g/dL + 0.6 x [Pi] mg/dL– BB = -24.6 mEq/L- 2.8 x 4.4 g/dL – 0.6 x (3.6 mg/dL)= -39• Figge-Fencl algorithm– http://www.figge-fencl.org/
    • 22. Δ SID Δ buffer base• A change in SID forces a change in bufferbase• Displacement from normal (+39 mEq/L)quantitates metabolic acid-base disorders• PCO2 independent indexSinger RB, Hastings AB. Medicine 1948; 27: 223-242
    • 23. 20406080100120140160mEq/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -116HCO3 = -15.8A- = -13.20Buffer Base = -29SID = +29( 10)pH = 7.209PCO2 = 40 mm HgBEp = -10 mE/LSBE = -11 mEq/LANG = 11 mEq/LSIG = 5 mEq/LHyperchloremic Metabolic Acidosis
    • 24. Buffer Base (BB) in HyperchloremiaHCO3- = - 24.6 mEq/LAlbumin +PI = -14.4 mEq/LHCO3- = -15.8Albumin + PI = -13.2BB = -39 mEq/L andBB = -29 mEq/L and Cl- = 116H+ +HCO3- H2CO3 CO2 +H2OBEp = -10 mEq/L
    • 25. 20406080100120140160mmol/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -106HCO3- = -15.8Alb- + PI = -13.20Buffer Base = -29SID = +29Lactic Acidosis (Lactate- = 10 mmol/L)pH = 7.208PCO2 = 40 mm HgBEp = -10 mmol/LLac- = -10
    • 26. 20406080100120140160mmol/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -106HCO3- = -15.8Alb- + PI = -13.20Buffer Base = -29SID = +29Ketoacidosis (Ketones- = 10 mmol/L)pH = 7.208PCO2 = 40 mm HgBEp = -10 mmol/LKet- = -10
    • 27. 20406080100120140160mmol/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -116HCO3- = -15.8Alb- + PI = -13.20Buffer Base = -29SID = +29Hyperchloremic Phase of DKA( 10)pH = 7.208PCO2 = 40 mm HgBEp = -10 mmol/L
    • 28. 20406080100120140160mEq/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -96HCO3 = -33.8A- = -15.20Buffer Base = - 49SID = +49( 10)pH = 7.54PCO2 = 40 mm HgBEp = 10 mEq/LSBE = 11 mEq/LANG = 13Hypochloremic Metabolic Alkalosis
    • 29. 6.86.977.17.27.37.47.57.615 20 25 30 35 40 45 50 55pHSID (mEq/L)pH = 7.4PaCO2 = 40 mm HgSID = 39 mEq/LAT = Standard State+-pH as a function of SID
    • 30. Etiology of Metabolic Acid-BaseDisturbances• Changes in Strong Ion Difference– Increased = Metabolic Alkalosis• Excess of plasma cations– Reduced = Metabolic Acidosis• Excess of plasma anions*Summarizes Acid-Base Status Circa 1962
    • 31. Plasma Base Excess0102030405060708090-20 -15 -10 -5 0 5 10 15 20 25Plasma Base Excess (mEq/L)H+(nM/L)*Summarizes Acid-Base Status Circa 196224 29 34 39 44 49 54SID (mEq/L)
    • 32. – Excess Anions < -2 mMol/L (Metabolic Acidosis)– Excess Cations > +2 mMol/L (Metabolic Alkalosis)– Change from 39 reflects of degree of anion /cation disparity only regarding strong ions– Magnitude of metabolic component of acid-basestatus in plasma compartment• Not Standard Base Excess (SBE)– PCO2 independent indexBE Scale for Metabolic Acid-Base Disorders*Siggard-Anderson O. Scand J Clin Lab Invest 1962; 14: 598-604
    • 33. • {+} value• excess plasma cations = metabolic alkalosis• {-} value• excess plasma anions = metabolic acidosis• Magnitude of metabolic component of acid-basestatus in extracellular fluid compartment• Adjusts for Gibbs Donnan effect unlike BEp• Metabolic Acidosis• PCO2 = SBE then normal compensation• Respiratory acidosis/alkalosis (pure)• SBE = 0• PCO2 independent indexStandard Base Excess
    • 34. Which profile has the most severemetabolic acid-base derangement?• A. pH = 7.19, PCO2 = 40, HCO3 = 15• B. pH = 7.55, PCO2 = 18, HCO3 = 15• C. pH = 7.10, PCO2 = 74, HCO3 = 22
    • 35. Which profile has the most severemetabolic acid-base derangement?• A. pH = 7.19, PCO2 = 40, HCO3 = 15– SBE = -11.6 mmol/L• B. pH = 7.55, PCO2 = 18, HCO3 = 15– SBE = -6.6 mmol/L• C. pH = 7.10, PCO2 = 74, HCO3 = 22– SBE = -6.4 mmol/L
    • 36. Dehydration• Dehydration and Water intoxication– Water loss/gain from intracellular and interstitialcompartments– Associated with hypertonicity/hypotonicity andchanges in plasma [Na+] (excludes uremia, DKA,NKHC, mannitol…)– Symptoms: thirst, confusion, coma– Quantitatively described as free water deficiency/excess• Volume of water that must be removed/added tohypotonic/hypertonic plasma to make isotonic plasma– Treatment: D5W with electrolytes, diuretics, andhypertonic salineLanguage Guiding Therapy: The Case of Dehydration versus Volume DepletionAnn Intern Med 1997;127:848-853
    • 37. • Volume depletion/expansion (hypo and hypervolemia)– Extracellular fluid compartment volume depletion/excessthat affects the vascular tree– Surrogate term for where cardiac function lies on theStarling Curve– Diagnosis:• Macrocirculation Impairment: BP, HR, Orthostatics• Microcirculation Impairment: Lactic Acidosis, Low venous Svo2– Treatment: Crystalloids, Colloids, PRBC, or diureticsVolume Depletion
    • 38. Dehydration versus Volume Depletion• Changes in extracellular and intracellularcompartment volumes can be and often aredissociated• Indiscriminate use of the terms dehydration andvolume depletion risks confusion andtherapeutic errors
    • 39. Treatment of Dehydration Versus HypovolemiaLanguage Guiding Therapy: The Case of Dehydration versus Volume DepletionAnn Intern Med 1997;127:848-853
    • 40. Free Water Excess/Deficit effects on [Cl-]• Free H2O abnormality detected as an abnormal [Na+]– Plasma [Cl-] has to be corrected for the dilution orconcentration of plasma [Na+]– [Cl-] predicted = [Cl-] normal x [Na+] observed / [Na+] normal– If plasma [Na+] =155 mmol/L• Then [Cl-] = 106 x 155/142 = 115 mmol/L– If plasma [Na+] =131 mmol/L• Then [Cl-] = 106 x 131/142 = 97 mmol/L
    • 41. Free H2O excess/deficit effects on Plasma [Na+]-3 L 155 115 +3 (42)-2 L 150 111 +2 (41)-1 L 146 108 +1 (40)0 142 105 0 (39)+1 L 138 102 -1 (38)+2 L 134 99 -2 (37)+3 L 131 97 -3 (36)Free H2O [Na+] [Cl-]  SID/SIDStandard StateNguyen M. and Kurtz I: J Applied Physiology 2006; 100: 1293–1300ConcentrationalAlkalosisDilutionalAcidosis
    • 42. Sodium 134 mEq/LPotassium 3.8 mEq/LChloride 83 mEq/LBicarbonate 24 mEq/LPO2 89 mm HgPCO2 32 mm HgpH 7.48Which of the following is the most likely explanation for these laboratoryfindings?(A) Respiratory alkalosis(B) Respiratory alkalosis and metabolic acidosis(C) Metabolic acidosis(D) Respiratory alkalosis, metabolic acidosis, and metabolic alkalosis(E) Metabolic alkalosis, respiratory alkalosis, and respiratory acidosisCl-(corrected) =106 x 134/142=100 mEq/LCl-(observed) = 83 mEq/L17 mEq/L excess cationsBEp = +17 strong cationsANGcorr = 33 or -17 anionsA 34-year-old white man presents with nausea, vomiting and has been unable toconsume 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 minutestanding, respirations are 24 per minute, and blood pressure is 110/85 mm Hgsupine and 80/50 mm Hg when standing.
    • 43. • Changes in Strong Ion Difference– Increased = Metabolic Alkalosis• Excess of plasma cations– Reduced = Metabolic Acidosis• Excess of plasma anions• Water deficit/excess:• Hypernatremia = Alkalosis (Cation Excess)• Hyponatremia = Acidosis (Cation Deficient)• Cation/Anion Imbalance• Hypochloremia = alkalosis (Anion Deficient)• Hyperchloremia = acidosis (Anion Excess)• Organic Acids (lactate, Ketones…) = acidosis– Anion ExcessEtiology of Metabolic Acid-Base Disturbances*Summarizes Acid-Base Status Circa 1962
    • 44. 20406080100120140160mmol/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -106HCO3- = -24.6Alb- + PI = -14.40Buffer Base = -39SID = +39Standard Physiologic State[Pi] = 3.6 mg/dLpH = 7.40PCO2 = 40 mm HgBEp = 0 mEq/L
    • 45. 20406080100120140160mmol/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -106HCO3- = -21.2Alb- + PI = -17.80Buffer Base = -39SID = +39Hyperphosphatemic Metabolic Acidosis[Pi] = 10 mg/dLpH = 7.337PCO2 = 40 mm HgBEp = -3.7 mEq/L
    • 46. 20406080100120140160mEq/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -106HCO3- = - 36.3A- = - 2.70Buffer Base = -39SID = +39Standard State Acid Base Status[Alb-] = 0 mg/dLpH = 7.571PCO2 = 40 mm HgBEp = 13 mEq/LSBE = 13 mEq/LANG = 1
    • 47. pH As A Function of Serum AlbuminConcentration7.357.47.457.57.551 1.5 2 2.5 3 3.5 4 4.5 5Albumin (g/dL)pHFIXEDSID = 39 mEq/LPCO2 = 40 mm HgPhosphate = 3.6 mg/dLFencl V, Rossing TH. Ann Rev Med 1989; 40:17-29
    • 48. Hyperchloremic Acidosis[Alb-] = 4.4 gm/dL20406080100120140160mmol/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -115HCO3- = - 15.8Alb- + PI = - 13.20Buffer Base = -29SID = +29( 10)pH = 7.208PCO2 = 40 mm HgBEp = -10 mEq/L
    • 49. 20406080100120140160mEq/LCations AnionsNa+ = 142K+ Ca++ Mg++Cl- = -116HCO3 = - 21.2A- = - 7.80Buffer Base = -29SID = +29( 10)pH = 7.338PCO2 = 40 mm HgSBE = - 4 mEq/LANG = 6 mEq/LAdj. ANG = 12 mEq/LSIG = 5 mEq/LHyperchloremic strong ion acidosis with concurrenthypoalbuminemic alkalosis ([albumin] = 2g/dL)
    • 50. Hypoalbuminemic AlkalosisHCO3- = -15.8 mEq/LCharge =-13.2 mEq/LHCO3- = -21.2 mEq/LAlbumin2.0 g/dLBB = -29 BB = -29H+ +HCO3- H2CO3 CO2 +H2OAlbumin4.4 g/dL Charge =-7.8 mEq/L
    • 51. Hypoalbuminemia- an adaptive response• Hypoalbuminemia independent risk factor• Beneficial by restoring pH towards normal• SBE = -10 mmol/L (Lactate = 10 mmol/L)[Albumin-] = 4.4 g/dL, pH = 7.202.2 g/dL, pH = 7.331.1 g/dL, pH = 7.38J Appl Physiol 1986; 61: 2260-2265
    • 52. pH as a Function of [Alb] and SID6.877.27.47.615 20 25 30 35 40 45 50 55SID (mEq/L)pH1.1 2.2 4.4Albumin (g/dL) =7.207.337.38
    • 53. AlbuminAlbumin• Major nonvolatile plasma weak acid buffer– (4 - 4.4 g/dL in plasma)• 1 gm = 2.8 mEq of acid• Accounts for 12.5 mEq/L of plasma fixed acid– Hypoalbuminemia = alkalosis– Hyperalbuminemia = acidosis– Loss of weak acid = gain in basic equivalentsJ Appl Physiol 1986; 61: 2260-2265
    • 54. • Hypoalbuminemia pervasive in acute illnessand surgery• Hypoalbuminemic alkalosis exists to someextent in all critically ill patients• Hypoalbuminemia corrects pH towardsstandard state in acute illnessAm J Respir Crit Care Med 2000; 162: 2246-2251
    • 55. • Changes in Strong Ion Difference– Increased = Metabolic Alkalosis• Excess of plasma cations– Reduced = Metabolic Acidosis• Excess of plasma anions• Water deficit/excess:• Hypernatremia = Alkalosis (Cation Excess)• Hyponatremia = Acidosis (Cation Deficient)• Cation/Anion Imbalance• Hypochloremia = alkalosis (Anion Deficient)• Hyperchloremia = acidosis (Anion Excess)• Organic Acids (lactate, Ketones…) = acidosis– Anion Excess• Abnormal concentrations of plasma weak acids– Independent determinants of pH– Hypoalbuminemia = metabolic alkalosis– Hyperalbuminemia = metabolic acidosis– Hyperphosphatemia = metabolic acidosisEtiology of Metabolic Acid-BaseDisturbances*Summarizes Acid-Base Status Circa 1982
    • 56. Am J Respir Crit Care Med Vol 162. pp 2246–2251, 2000
    • 57. Anion Gap (1977)• Law of electrical neutrality– Discrepancy between cations and anions virtual– Na+ + K+ = Cl- + HCO3- + XA-– (Na+ + K+ - Cl- - HCO3)  16– Facilitates differential diagnosis (easy to compute)– Normal ANG entirely accounted for by [albumin] + PI– ANG = 2.8*Albumin + 0.5 *PI– Very Unreliable in critical illness• Hypoalbuminemia• pH changes• Gibbs Donnan EffectOh MS & Carroll HJ. The Anion Gap. NEJM 1977; 297: 814-817.
    • 58. 20406080100120140160mEq/LCations AnionsNa+ = 142K+ = 4Cl- = -105HCO3 = -24.6A- = -14.40pH = 7.40PCO2 = 40 mm HgSBE = 0 mEq/LANG = 12 mEq/LSIG = 5 mEq/LXA-XA- = Unmeasured Anions:CyanideGlycolsIronIsoniazidKetoacidsKrebs CycleLactateMethanolParaldehydeTolueneSalicylateUremiaANGAnion Gap
    • 59. 68 yo male UGI BleedNa =132, K = 4, Cl = 98, HCO3 = 22Lactate = 4.5, Alb = 2.8ANG = Na + K – Cl – HCO3 = 16 (“normal”)ANG(c) = 16 + 2.8(4.4 - 2.8) = 20.5 (abnormal)WHY?Adding back lost charge from hypoalbuminemiaAnion gap and hypoalbuminemia. Crit Care Med. 1998 Nov;26(11):1807–1810
    • 60. Anion Gap as function of AlbuminConcentration468101214161 1.5 2 2.5 3 3.5 4 4.5 5Albumin (g/dL)AnionGap(mEq/L)Fencl V, Rossing TH. Ann Rev Med 1989; 40:17-29Anion Gap = ( Na+ + K+ – Cl- – HCO3-)
    • 61. Anion Gap as a function of pH1112131415166.8 7 7.2 7.4 7.6pHAnionGapAnion Gap = ( Na+ + K+ – Cl- – HCO3-)
    • 62. Anion GapAnion Gap• Insensitive index of organic acidosis in acuteillness and post surgery (hypoalbuminemia, pHeffects)• Adjusted Anion Gap for hypoalbuminemia= ANG + 2.8( 4.4 - Observed alb.)Increased anion gap = acidosisDecreased anion gap = alkalosis
    • 63. Strong Ion Gap• Unmeasured Anions of Critical Illness– All organic anions (ketones, lactate …)• Codeterminants of Strong Ion Difference– SIG = SID(apparent) – Buffer Base– SIDa = Na+ + K+ +Ca+++ Mg++ - Cl- - Lactate-• Not affected by pH or [Albumin]• Equivalent to the Anion Gap (corrected)
    • 64. 20406080100120140mmol/LCations AnionsNa+ = 142 Cl- = -106HCO3- = -24.6Alb- + PI = -14.40Strong Ion Gap: SIDa – BB = SIGpH = 7.40PCO2 = 40 mm HgBEp = 0 mmol/LXA-K+ Ca2+ Mg2+Lactate-SIDaBuffer BaseStrong Ion GapSIDa = Na+ + K+ + Ca2+ + Mg2+ - Cl- - lactate- - XA-
    • 65. 20406080100120140160mEq/LCations AnionsNa+ = 142K+ = 4Cl- = -105HCO3A-0pH = 7.40PCO2 = 40 mm HgSBE = 0 mEq/LANG = 12 mEq/LSIG = 5 mEq/LXA-SIDaStrong Ion GapSIDe or Buffer BaseStrong Ion Gap
    • 66. Calculation of the SID and apparent SID• Buffer Base  [HCO3-] + 2.8 x [Alb-] g/dL + 0.6 x [Pi] mg/dL– BB = -24.6 mEq/L- 2.8 x 4.4 g/dL – 0.6 x (3.6 mg/dL)= -39• SIDa  Na+ + K+ + (Mg2+ + Ca 2+) - Cl- - lactate-– SIDa  Na+ + K+ + 3 – Cl- - lactate- = 42 mEq/L• SIG = SIDa – Buffer Base• SIG = 42 – 39  3 mEq/L
    • 67. Independent Determinants of pH• Strong Ion Difference (SID)• Strong Ion Gap• Plasma Weak Acids• CO2 production• This is physico-chemical analysis!
    • 68. Physico-Chemical Analysis• Three independent determinants of acid-basestatus– Strong Ion Difference– PCO2– Variable weak acid total ([albumin-] + PI)• Mechanistic and quantitative• Guides diagnosis and therapyStewart P. Can J. Physiol. Pharmacology 1983; 61: 1444-1461
    • 69. Normal Saline Lactated Ringers 1/2 NS with 75 mEq/L NaHCO3 NaHCO3Na 154 130 150 150K 4MgCa 3Cl 154 109 75AcetateGluconateLactate 28SID 0 28 75 150*Caution must be exercised in patients with acute or chronic renal failureand K containing solutions (LR)*NaHCO3 solution: 3 Amps NaHCO3 in 1 Liter sterile water or D5WIsotonic Crystalloid Solutions-1.8 SBE/L +0.4 SBE/L +4 SBE/L +9 SBE/L
    • 70. Crystalloid SID and serum [HCO3-]• If crystalloid SID  plasma [HCO3-] (24.6 mmol/L)– No change in SBE or acid-base status– Lactated Ringer’s, Hartman’s Solution, Hextend• If crystalloid SID < plasma [HCO3-]– Metabolic acidosis– Normal Saline• If crystalloid SID > plasma [HCO3-]– Metabolic alkalosis– Plasmalyte, ½ NS + 75 mEq/L NaHCO3, and isotonicbicarbonate solutionsOmron E: J Int Care Med 2010. 25; 271-280
    • 71. Metabolic Acid-Base Effects of Crystalloid Infusion-15-10-505101520253035400 1 2 3 4 5 6 7 8 9 10Crystalloid Infusion Volume (Liters)SBEmEq/LNormal Saline (SID = 0)Crystalloid SID = 24.5 mEq/LRingers Lactate (SID = 28)Plasmalyte 148 (SID = 50)1/2 NS + 75 mEq/L NaHCO3 (SID = 75)0.15 M NaHCO3 (SID = 150)Omron E: J Int Care Med 2010. 25; 271-280
    • 72. Physicochemical Resuscitation• Principles– Patients in shock with a metabolic acidosis areoptimally managed with isotonic crystalloidsolutions that are alkaline when infused– Patients with normal acid base status are bestmanaged with isotonic balanced solutions– Patients with metabolic alkalosis are optimallymanaged with isotonic solutions that are acidicwhen infused– The principles of Early Goal Directed Therapy areto be done concurrently with physicochemicalresuscitation
    • 73. Crystalloid Resuscitation Guidelines at albumin = 2.2 g/dL0102030405060708090-20 -15 -10 -5 0 5 10 15 20 25SBE (mEq/L)H+(nM/L)0**344 0**0**1**2 10 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid1 = Normal Saline (SID = 0), 1.8 mmol/L acid2 = Lactated Ringers ( SID = 28), 0.4 mmol/L base3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base4 = 3 Amps NaHCO3 in sterile H20 in 1 liter (SID = +150), 9 mmol/L base Edward Omron MD, MPH** Acetazolamide 250 mg IVP q12, no more than 500 mg qday Pulmonary / Critical CareDialysis
    • 74. Isotonic (Normal) Saline• 0.9% Sodium Chloride in sterile water• Na+ = 154 mmol/L, Cl- = 154 mmol/L• SID = 0• Excellent choice in– Hypovolemic, Hypochloremia with metabolic alkalosis– SBE ≥ 0• 1.8 mmol/L fixed acid generated (excess Cl-)• -1.8 SBE/Liter infused
    • 75. Lactated Ringer’s Solution• Polyionic isotonic crystalloid that mimics plasmaelectrolyte concentration• Na+ = 130, K+=4, Cl- = 109, Lact- = 28, Ca++ = 3• SID = 28• Excellent choice in mild metabolic acidosis withpreserved renal function (SBE = -5 to +5)• 0.4 mmol/L fixed base• 0.4 SBE/Liter infused
    • 76. 1/2 NS with 75 mEq/L HCO3• 1/2 NS + 1.5 Amps Na HCO3 per liter• Isotonic resuscitation and maintenance• Na+ =150 mmol/L, Cl- = 75 mmol/L HCO3 = 75mmol/L• SID = +75• Hyperchloremic metabolic acidosis and reducedrenal function Plasma SBE -10 to -5• 4 mmol fixed base/Liter infused• +4 SBE/ Liter
    • 77. Isotonic NaHCO3- Administration• 3 Amps Na HCO3 in 1 liter sterile H2O• Isotonic Resuscitation and maintenance• Na+ = 150, HCO3 = 150• SID = 150• Excellent choice in malignant acidemias• Bridge to acute dialysis: SBE ≤ -10• +9 mmol fixed base/ Liter infused• +9 SBE/Liter
    • 78. Metabolic Acid-Base Effects of Crystalloid Infusionduring moderate metabolic acidosis-15-10-50510150 1 2 3 4 5Crystalloid Infusion Volume (Liters)SBEmEq/LNormal SalineCrystalloid SID = 20 mEq/LRingers LactatePlasmalyte1/2 NS + 75 mEq/L NaHCO30.15 M NaHCO3Omron E: J Int Care Med 2010. 25; 271-280
    • 79. • Assumptions– Normal renal function– Acute and chronic kidney injury resultin marked impairment in chlorideexcretion– VD may change in acute illness andsurgery– Ignores the effects of tissue buffering
    • 80. Bicarbonate Solutions• Historically: hyperosmolar solution– 1 amp = 50 mEq/50 cc or 1 mEq/cc (1 M)– Correction of extracellular acidosis at theexpense of massive intracellular derangement– No defined physico-chemical endpoint– Hypertonic volume expansion• Recently shown to increase mortality in shock– Only use isotonic solutions: Sterile water orD5W + 3 amps Na HCO3! (0.15 M)– Activates Phosphofructokinase !– Aggravates minute ventilation !
    • 81. Alkalosis activates PFK**Aggravates lactic acidosis in shock states
    • 82. 28 yo male with ARDS undergoingdiuresis• pH = 7.61, PaCO2 = 40 mm Hg,• [HCO3-]HH = 39.4 mmol/L,• SBE = 16.8 mmol/L• Na+ = 144 mmol/L, Cl- = 91 mmol/L• Cl- corrected = 106 x 144/142 = 107– Cl- loss 16 mmol/L ( 107-91) = 16 mmol/L excess cations• Severe hypochloremic metabolic alkalosis– Mechanism?– Treatment?
    • 83. Crystalloid Resuscitation Guidelines at albumin = 2.2 g/dL0102030405060708090-20 -15 -10 -5 0 5 10 15 20 25SBE (mEq/L)H+(nM/L)0**344 0**0**1**2 10 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid1 = Normal Saline (SID = 0), 1.8 mmol/L acid2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base4 = 3 Amps NaHCO3 in sterile H20 in 1 liter (SID = +150), 9 mmol/L base Edward Omron MD, MPH** Acetazolamide 250 mg IVP q12, no more than 500 mg qd Pulmonary / Critical CareDialysis
    • 84. 67 yo female with ischemic bowel• BP 80/40, HR 120, HCT= 25• pH = 7.26, PaCO2 = 24, HCO3 = 11,• SBE = -14.6• Na+ = 143, Cl- = 118• Cl- corrected = 106 x 143/142  106• Excess Cl- (118 - 106) = 12 mmol/L• Mechanism: Hyperchloremia• How do you fix?What are the resuscitation fluids of choice?
    • 85. Crystalloid Resuscitation Guidelines at albumin = 2.2 g/dL0102030405060708090-20 -15 -10 -5 0 5 10 15 20 25SBE (mEq/L)H+(nM/L)0**344 0**0**1**2 10 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid1 = Normal Saline (SID = 0), 1.8 mmol/L acid2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base4 = 3 Amps NaHCO3 in sterile H20 in 1 liter (SID = +150), 9 mmol/L base Edward Omron MD, MPH** Acetazolamide 250 mg IVP q12, no more than 500 mg qd Pulmonary / Critical CareDialysis
    • 86. 78 yo with severe pneumonia andsepsis• pH=7.37, PCO2=26.9, HCO3=15.2,• SBE = -9,• Na = 134 and Cl = 113 and albumin = 3 g/dL• Cl- corrected = 106 x 134/142 = 100 mmol/L– Excess chloride = 13 mmol/L• Mechanism of metabolic acidosis– Hyperchloremia– Free water excess reducing Na• Hypoalbuminemic Alkalosis• How do you fix?• Resuscitation Fluid?
    • 87. Crystalloid Resuscitation Guidelines at albumin = 2.2 g/dL0102030405060708090-20 -15 -10 -5 0 5 10 15 20 25SBE (mEq/L)H+(nM/L)0**344 0**0**1**2 10 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid1 = Normal Saline (SID = 0), 1.8 mmol/L acid2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base4 = 3 Amps NaHCO3 in sterile H20 in 1 liter (SID = +150), 9 mmol/L base Edward Omron MD, MPH** Acetazolamide 250 mg IVP q12, no more than 500 mg qd Pulmonary / Critical CareDialysis
    • 88. Additional Referenceshttp://www.slideshare.net/edofironwww.acidbase.orghttp://www.figge-fencl.org/Intensive Care Medicine 2011. 37; 461-468.J. Intensive Care Medicine 2010. 25; 271-280.Intensive Care Medicine 2009. 35; 1377-1382.Critical Care Medicine 2005. 21; 329-346.Best Practice Res Clin Anes 2004. 18; 113-127.Kidney Inter. 2003. 64; 777-787.Am. J. Respir. Crit. Care Med. 2000. 162; 2246-2251.J. Applied Physiology 1999. 86; 326-334.Annual Review Medicine 1989. 40; 17-29.