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

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 ...

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

    • A Primer of Acid-Base Assessment by Physicochemical Analysis and Strong Ion Difference
      Edward M. Omron MD, MPH, FCCP
      Pulmonary and Critical Care Medicine
      edofiron@gmail.com
    • OBJECTIVES
      A critical assessment of conventional acid-base analysis
      A review of strong ion difference and physicochemical analysis in acute illness and major surgery
      Clinical applications in
      Electrolyte management
      Fluid resuscitation
      Complex acid-base disorders
    • Metabolic acid-base status
      What is it?
      Why is it important?
      Why assess for it?
      Can we do better?
    • 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.
      Which of the following is the most likely explanation for these laboratory findings?
      (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
    • Concept of pH
      pH H+
      • 7.0 100 nmol/L
      • 7.4 40
      • 7.7 20
      pH = - log (H+): log linear
      Exponential in reality
    • “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.”
      Henderson LJ; Science 1917;46:73-83
    • Figure 1. Henderson-Hasselbalch Equations
      H+ + HCO3- H2CO3 CO2 + H2O
      • [H+] = 24 x PCO2/[HCO3-]
      • pH = 6.1 + Log [HCO3-] / [0.03 x PCO2]
      pK = 6.1
    • 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 and pH
      Slope = -1
    • In-Vitro
    • Gibbs Donnan Effect
    • Gibbs Donnan Effect
      Constable P. J Appl Physiol 1997; 83(1): 298
    • 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
    • Charge Balance at Standard Physiologic State
      160
      K+ Ca++ Mg++
      140
      SID = +39
      120
      mmol/L
      100
      80
      Cl- = -106
      Na+ = 142
      60
      40
      20
      0
      Cations
      Anions
    • Charge Balance at Standard Physiologic State
      160
      K+ Ca++ Mg++
      140
      A- = -14.4
      SID = +39
      Buffer Base = -39
      120
      HCO3 = -24.6
      mEq/L
      100
      80
      Cl- = -106
      Na+ = 142
      60
      pH = 7.40
      PaCO2 = 40 mm Hg
      BEp = 0 mEq/L
      SBE = 0 mEq/L
      ANG = 12 mEq/L
      SIG = 5 mEq/L
      40
      20
      0
      Cations
      Anions
    • Strong Ions and Charge Balance
      Na+ + 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 = ?-39
      Strong Ion Difference = Buffer Base
    • 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 Citrate
      J Appl Physiol 1986; 61: 2260-2265
    • Standard physiological state in plasma for 70 kg test subject (TBW = 60% total body weight)
      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
    • 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/
    • Δ SID Δ buffer base
      A change in SID forces a change in buffer base
      Displacement from normal (+39 mEq/L) quantitates metabolic acid-base disorders
      PCO2 independent index
      Singer RB, Hastings AB. Medicine 1948; 27: 223-242
    • Hyperchloremic Metabolic Acidosis
      160
      K+ Ca++ Mg++
      140
      A- = -13.2
      Buffer Base = -29
      SID = +29
      120
      HCO3= -15.8
      mEq/L
      100
      80
      ( 10)
      Cl- = -116
      Na+ = 142
      60
      pH = 7.209
      PCO2 = 40 mm Hg
      BEp = -10 mE/L
      SBE = -11 mEq/L
      ANG = 11 mEq/L
      SIG = 5 mEq/L
      40
      20
      0
      Cations
      Anions
    • Buffer Base (BB) in Hyperchloremia
      BB = -39 mEq/L and Cl- = 106
      BB = -29 mEq/L and Cl- = 116
      HCO3- = - 24.6mEq/L
      HCO3- = -15.8
      Albumin + PI = -13.2
      Albumin +PI = -14.4 mEq/L
      H+ +HCO3- H2CO3 CO2 +H2O
      BEp = -10 mEq/L
    • Lactic Acidosis (Lactate- = 10 mmol/L)
      160
      K+ Ca++ Mg++
      140
      Alb- + PI= -13.2
      SID = +29
      Buffer Base = -29
      HCO3-= -15.8
      120
      Lac- = -10
      mmol/L
      100
      80
      Cl- = -106
      Na+ = 142
      60
      40
      pH = 7.208
      PCO2 = 40 mm Hg
      BEp = -10 mmol/L
      20
      0
      Cations
      Anions
    • Ketoacidosis (Ketones- = 10 mmol/L)
      160
      K+ Ca++ Mg++
      140
      Alb- + PI= -13.2
      SID = +29
      Buffer Base = -29
      HCO3-= -15.8
      120
      Ket- = -10
      mmol/L
      100
      80
      Cl- = -106
      Na+ = 142
      60
      40
      pH = 7.208
      PCO2 = 40 mm Hg
      BEp = -10 mmol/L
      20
      0
      Cations
      Anions
    • Hyperchloremic Phase of DKA
      160
      K+ Ca++ Mg++
      140
      Alb- + PI= -13.2
      SID = +29
      Buffer Base = -29
      120
      HCO3-= -15.8
      mmol/L
      100
      80
      ( 10)
      Cl- = -116
      Na+ = 142
      60
      40
      pH = 7.208
      PCO2 = 40 mm Hg
      BEp = -10 mmol/L
      20
      0
      Cations
      Anions
    • Hypochloremic Metabolic Alkalosis
      160
      K+ Ca++ Mg++
      140
      A- = -15.2
      Buffer Base = - 49
      SID = +49
      120
      HCO3= -33.8
      100
      mEq/L
      80
      ( 10)
      Cl- = -96
      Na+ = 142
      60
      pH = 7.54
      PCO2 = 40 mm Hg
      BEp = 10 mEq/L
      SBE = 11 mEq/L
      ANG = 13
      40
      20
      0
      Cations
      Anions
    • pH as a function of SID
      -
      +
    • Etiology of Metabolic Acid-Base Disturbances
      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
    • 24 29 34 39 44 49 54
      SID (mEq/L)
      *Summarizes Acid-Base Status Circa 1962
    • BE Scale for Metabolic Acid-Base Disorders
      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-base status in plasma compartment
      Not Standard Base Excess (SBE)
      PCO2 independent index
      *Siggard-Anderson O. Scand J Clin Lab Invest 1962; 14: 598-604
    • Standard Base Excess
      • {+} value
      excess plasma cations = metabolic alkalosis
      • {-} value
      excess plasma anions = metabolic acidosis
      • Magnitude of metabolic component of acid-base status 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 index
    • Which profile has the most severe metabolic 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
    • Which profile has the most severe metabolic 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
    • Dehydration
      Dehydration and Water intoxication
      Water loss/gain from intracellular and interstitial compartments
      Associated with hypertonicity/hypotonicity and changes 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 to hypotonic/hypertonic plasma to make isotonic plasma
      Treatment: D5W with electrolytes, diuretics, and hypertonic saline
      Language Guiding Therapy: The Case of Dehydration versus Volume Depletion
      Ann Intern Med 1997;127:848-853
    • Volume Depletion
      Volume depletion/expansion (hypo and hypervolemia)
      Extracellular fluid compartment volume depletion/excess that affects the vascular tree
      Surrogate term for where cardiac function lies on the Starling Curve
      Diagnosis:
      Macrocirculation Impairment: BP, HR, Orthostatics
      Microcirculation Impairment: Lactic Acidosis, Low venous Svo2
      Treatment: Crystalloids, Colloids, PRBC, or diuretics
    • Dehydration versus Volume Depletion
      Changes in extracellular and intracellular compartment volumes can be and often are dissociated
      Indiscriminate use of the terms dehydration and volume depletion risks confusion and therapeutic errors
    • Treatment of Dehydration Versus Hypovolemia
      Language Guiding Therapy: The Case of Dehydration versus Volume Depletion
      Ann Intern Med 1997;127:848-853
    • Free Water Excess/Deficit effects on [Cl-]
      Free H2O abnormality detected as an abnormal [Na+]
      Plasma [Cl-] has to be corrected for the dilution or concentration 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
    • Free H2O excess/deficit effects on Plasma [Na+]
      Free H2O [Na+] [Cl-]  SID/SID
      Concentrational
      Alkalosis
      Standard State
      Dilutional Acidosis
      Nguyen M. and Kurtz I: J Applied Physiology 2006; 100: 1293–1300
    • 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.
      Cl-(corrected) =106 x 134/142
      =100 mEq/L
      Cl-(observed) = 83 mEq/L
      17 mEq/L excess cations
      BEp = +17 strong cations
      ANGcorr = 33 or -17 anions
      Which of the following is the most likely explanation for these laboratory findings?
      (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
    • Etiology of Metabolic Acid-Base Disturbances
      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
      *Summarizes Acid-Base Status Circa 1962
    • Standard Physiologic State [Pi] = 3.6 mg/dL
      160
      K+ Ca++ Mg++
      140
      Alb- + PI= -14.4
      SID = +39
      Buffer Base = -39
      120
      HCO3-= -24.6
      mmol/L
      100
      80
      Cl- = -106
      Na+ = 142
      60
      40
      pH = 7.40
      PCO2 = 40 mm Hg
      BEp = 0 mEq/L
      20
      0
      Cations
      Anions
    • Hyperphosphatemic Metabolic Acidosis [Pi] = 10 mg/dL
      160
      K+ Ca++ Mg++
      140
      Alb- + PI= -17.8
      SID = +39
      Buffer Base = -39
      120
      HCO3-= -21.2
      mmol/L
      100
      80
      Cl- = -106
      Na+ = 142
      60
      40
      pH = 7.337
      PCO2 = 40 mm Hg
      BEp = -3.7 mEq/L
      20
      0
      Cations
      Anions
    • Standard State Acid Base Status
      [Alb-] = 0 mg/dL
      160
      K+ Ca++ Mg++
      140
      A-= - 2.7
      SID = +39
      Buffer Base = -39
      120
      HCO3-= - 36.3
      mEq/L
      100
      80
      Cl- = -106
      Na+ = 142
      60
      pH = 7.571
      PCO2 = 40 mm Hg
      BEp = 13 mEq/L
      SBE = 13 mEq/L
      ANG = 1
      40
      20
      0
      Cations
      Anions
    • Fencl V, Rossing TH. Ann Rev Med 1989; 40:17-29
    • Hyperchloremic Acidosis [Alb-] = 4.4 gm/dL
      160
      K+ Ca++ Mg++
      140
      Alb- + PI= - 13.2
      SID = +29
      Buffer Base = -29
      120
      HCO3-= - 15.8
      mmol/L
      100
      80
      ( 10)
      Cl- = -115
      Na+ = 142
      60
      40
      pH = 7.208
      PCO2 = 40 mm Hg
      BEp = -10 mEq/L
      20
      0
      Cations
      Anions
    • Hyperchloremic strong ion acidosis with concurrent hypoalbuminemic alkalosis ([albumin] = 2g/dL)
      160
      A- = - 7.8
      K+ Ca++ Mg++
      140
      Buffer Base = -29
      SID = +29
      HCO3= - 21.2
      120
      100
      mEq/L
      80
      ( 10)
      Cl- = -116
      Na+ = 142
      60
      pH = 7.338
      PCO2 = 40 mm Hg
      SBE = - 4 mEq/L
      ANG = 6 mEq/L
      Adj. ANG = 12 mEq/L
      SIG = 5 mEq/L
      40
      20
      0
      Cations
      Anions
    • Hypoalbuminemic Alkalosis
      BB = -29
      BB = -29
      HCO3- = -21.2 mEq/L
      HCO3- = -15.8mEq/L
      Albumin
      4.4 g/dL
      Charge = -13.2 mEq/L
      Charge =
      -7.8 mEq/L
      Albumin
      2.0 g/dL
      H+ +HCO3- H2CO3 CO2 +H2O
    • 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 = 7.20
      • 2.2 g/dL, pH = 7.33
      • 1.1 g/dL, pH = 7.38
      J Appl Physiol 1986; 61: 2260-2265
    • J Appl Physiol 1986; 61: 2260-2265
    • Hypoalbuminemia pervasive in acute illness and surgery
      Hypoalbuminemic alkalosis exists to some extent in all critically ill patients
      Hypoalbuminemia corrects pH towards standard state in acute illness
      Am J Respir Crit Care Med 2000; 162: 2246-2251
    • Etiology of Metabolic Acid-Base Disturbances
      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 acidosis
      *Summarizes Acid-Base Status Circa 1982
    • Am J Respir Crit Care Med Vol 162. pp 2246–2251, 2000
    • 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 Effect
      Oh MS & Carroll HJ. The Anion Gap. NEJM 1977; 297: 814-817.
    • Anion Gap
      XA-= Unmeasured Anions:
      Cyanide
      Glycols
      Iron
      Isoniazid
      Ketoacids
      Krebs Cycle
      Lactate
      Methanol
      Paraldehyde
      Toluene
      Salicylate
      Uremia
      160
      XA-
      K+ = 4
      140
      ANG
      A- = -14.4
      120
      HCO3= -24.6
      100
      mEq/L
      80
      Na+= 142
      Cl- = -105
      60
      pH = 7.40
      PCO2 = 40 mm Hg
      SBE = 0 mEq/L
      ANG = 12 mEq/L
      SIG = 5 mEq/L
      40
      20
      0
      Cations
      Anions
    • 68 yo male UGI Bleed
      Na =132, K = 4, Cl = 98, HCO3 = 22
      Lactate = 4.5, Alb = 2.8
      ANG = Na + K – Cl – HCO3 = 16 (“normal”)
      ANG(c) = 16 + 2.8(4.4 - 2.8) = 20.5 (abnormal)
      WHY?
      Adding back lost charge from hypoalbuminemia
      Anion gap and hypoalbuminemia. Crit Care Med. 1998 Nov;26(11):1807–1810
    • Anion Gap = ( Na+ + K+ – Cl- – HCO3-)
      Fencl V, Rossing TH. Ann Rev Med 1989; 40:17-29
    • Anion Gap = ( Na+ + K+ – Cl- – HCO3-)
    • 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)
    • Strong Ion Gap: SIDa – BB = SIG
      SIDa = Na+ + K+ + Ca2+ + Mg2+ - Cl- - lactate- - XA-
      Strong Ion Gap
      K+ Ca2+ Mg2+
      XA-
      140
      Alb- + PI= -14.4
      SIDa
      120
      Buffer Base
      HCO3-= -24.6
      mmol/L
      100
      Lactate-
      80
      Na+ = 142
      Cl- = -106
      60
      40
      pH = 7.40
      PCO2 = 40 mm Hg
      BEp = 0 mmol/L
      20
      0
      Cations
      Anions
    • Strong Ion Gap
      160
      XA-
      Strong Ion Gap
      K+ = 4
      140
      A-
      SIDa
      120
      SIDe or Buffer Base
      HCO3
      100
      mEq/L
      80
      Na+= 142
      Cl- = -106
      60
      pH = 7.40
      PCO2 = 40 mm Hg
      SBE = 0 mEq/L
      ANG = 12 mEq/L
      SIG = 5 mEq/L
      40
      20
      0
      Cations
      Anions
    • 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
    • Independent Determinants of pH
      Strong Ion Difference (SID)
      Strong Ion Gap
      Plasma Weak Acids
      CO2 production
      This is physico-chemical analysis!
    • Physico-Chemical Analysis
      Three independent determinants of acid-base status
      Strong Ion Difference
      PCO2
      Variable weak acid total ([albumin-] + PI)
      Mechanistic and quantitative
      Guides diagnosis and therapy
      Stewart P. Can J. Physiol. Pharmacology 1983; 61: 1444-1461
    • Isotonic Crystalloid Solutions
      -1.8 SBE/L +0.4 SBE/L +4 SBE/L +9 SBE/L
      *Caution must be exercised in patients with acute or chronic renal failure
      and K containing solutions (LR)
      *NaHCO3 solution: 3 Amps NaHCO3 in 1 Liter sterile water or D5W
    • 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 isotonic bicarbonate solutions
      Omron E: J Int Care Med 2010. 25; 271-280
    • Metabolic Acid-Base Effects of Crystalloid Infusion
      Omron E: J Int Care Med 2010. 25; 271-280
    • Physicochemical Resuscitation
      Principles
      Patients in shock with a metabolic acidosis are optimally managed with isotonic crystalloid solutions that are alkaline when infused
      Patients with normal acid base status are best managed with isotonic balanced solutions
      Patients with metabolic alkalosis are optimally managed with isotonic solutions that are acidic when infused
      The principles of Early Goal Directed Therapy are to be done concurrently with physicochemical resuscitation
    • Dialysis
      4
      4
      1**
      1
      0**
      3
      2
      0**
      0**
      0 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid
      1 = Normal Saline (SID = 0), 1.8 mmol/L acid
      2 = Lactated Ringers ( SID = 28), 0.4 mmol/L base
      3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base
      4 = 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 Care
    • 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
    • Lactated Ringer’s Solution
      Polyionic isotonic crystalloid that mimics plasma electrolyte concentration
      Na+ = 130, K+=4, Cl- = 109, Lact- = 28, Ca++ = 3
      SID = 28
      Excellent choice in mild metabolic acidosis with preserved renal function(SBE = -5 to +5)
      0.4 mmol/L fixed base
      0.4 SBE/Liter infused
    • 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 = 75 mmol/L
      SID = +75
      Hyperchloremic metabolic acidosis and reduced renal function Plasma SBE -10 to -5
      4 mmol fixed base/Liter infused
      +4 SBE/ Liter
    • 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
    • Metabolic Acid-Base Effects of Crystalloid Infusion during moderate metabolic acidosis
      Omron E: J Int Care Med 2010. 25; 271-280
    • Assumptions
      Normal renal function
      Acute and chronic kidney injury result in marked impairment in chloride excretion
      VD may change in acute illness and surgery
      Ignores the effects of tissue buffering
    • Bicarbonate Solutions
      Historically: hyperosmolar solution
      1 amp = 50 mEq/50 cc or 1 mEq/cc (1 M)
      Correction of extracellular acidosis at the expense 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 or D5W + 3 amps Na HCO3! (0.15 M)
      Activates Phosphofructokinase !
      Aggravates minute ventilation !
    • Alkalosis activates PFK
      **Aggravates lactic acidosis in shock states
    • 28 yo male with ARDS undergoing diuresis
      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?
    • Dialysis
      4
      4
      1**
      1
      0**
      3
      2
      0**
      0**
      0 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid
      1 = Normal Saline (SID = 0), 1.8 mmol/L acid
      2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base
      3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base
      4 = 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 Care
    • 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?
    • Dialysis
      4
      4
      1**
      1
      0**
      3
      2
      0**
      0**
      0 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid
      1 = Normal Saline (SID = 0), 1.8 mmol/L acid
      2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base
      3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base
      4 = 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 Care
    • 78 yo with severe pneumonia and sepsis
      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?
    • Dialysis
      4
      4
      1**
      1
      0**
      3
      2
      0**
      0**
      0 = HCl infusion (0.1 N) at 100 to 200 cc/ hr, central access (SID = -100), 3 mmol/L acid
      1 = Normal Saline (SID = 0), 1.8 mmol/L acid
      2 = Lactated Ringer’s( SID = 28), 0.4 mmol/L base
      3 = ½ NS with 75 mEq/L NaHCO3 in 1 liter (SID = +75), 4 mmol/L base
      4 = 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 Care
    • Additional References
      http://www.slideshare.net/edofiron
      www.acidbase.org
      http://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.