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New models of acid-basebalance and their application to critical care nephrology  (an abbreviated introduction to Stewart's model of acid base disturbances)
 

New models of acid-base balance and their application to critical care nephrology (an abbreviated introduction to Stewart's model of acid base disturbances)

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A short introduction to Stewart's model of acid-base disturbances. Modified from a talk I gave during a fellow's retreat back in 2006 in the beautiful Seven Spring's resort....

A short introduction to Stewart's model of acid-base disturbances. Modified from a talk I gave during a fellow's retreat back in 2006 in the beautiful Seven Spring's resort.

Will probably get excommunicated by the Nephrology Orthodoxy for endorsing Stewart's "heresy" :) but it is worth it!

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    New models of acid-basebalance and their application to critical care nephrology  (an abbreviated introduction to Stewart's model of acid base disturbances) New models of acid-base balance and their application to critical care nephrology (an abbreviated introduction to Stewart's model of acid base disturbances) Presentation Transcript

    • New models of acid-base balance and their application to critical care nephrology Christos Argyropoulos MD PhD Department of Internal Medicine, Renal and Electrolyte Division
    • Goals of acid-base models
      • P atient C are : diagnosis and treatment of complex acid-base disorders
      • Medical Education : establish the paradigm of acid-base physiology taught in medical curricul a
      • Research : Advance understanding of genetic disorders of ion transport in epithelial celss
    • Qualifications of an acid-base model (formal)
      • A general acid-base model should provide:
      • the classification of the disturbance as “metabolic” or “respiratory”
      • a mechanistic explanation for the underlying disturbance
      • a quantitative estimate of the magnitude of an acid-base disturbance
      • the enumeration of the independent variables that govern the disturbance.
    • Qualifications of an acid-base model (informal)
      • A general acid-base model should answer the following questions:
      • Which organ/system is causing the disturbance?
      • How does it cause the disturbance?
      • What is the magnitude of the disturbance
      • What should I do to fix this?
    • “ Standard” Model
      • Acid = H + donor, Base = H + acceptor
      • Final pH = function of amount of acid added or removed
      • Plasma membranes may be permeable to H +
      • Analysis of a single acid – base (HCO3 - /CO2) buffer system suffices to understand all disorders
      • Magnitude of disorder estimated by the Henderson Hasselbach equation
    • “ Standard” model or modelS ?
      • Magnitude of the disorder is used to decide mechanism/type/”dose” of therapy
      • Two main approaches to quantification:
        • The “six” rules of thumb (medicine boards a.k.a “Boston approach”)
        • Standard Base Excess and PCO2 (Anesthesia and Surgical boards aka “Copenhagen” approach)
    • Six rules of thumb
      • The 1 for 10 Rule for Acute Respiratory Acidosis
      • The 4 for 10 Rule for Chronic Respiratory Acidosis
      • The 2 for 10 Rule for Acute Respiratory Alkalosis
      • The 5 for 10 Rule for a Chronic Respiratory Alkalosis
      • The One & a Half plus 8 Rule - for a Metabolic Acidosis
      • The Point Seven plus Twenty Rule - for a Metabolic Alkalosis
    • Standard Base Excess
      • “ Amount of acid or base in meqs needed to titrate 1 lt of blood to pH 7.4 at pCO2 of 40mmHg keeping the temperature constant at 37 o C”
      • Calculated on the basis of modifications of the Van Slyke equation:
      • SBE = 0.9287 × (HCO3 – – 24.4 + 14.83 × [pH – 7.4])
      • “ SBE” = metabolic component, “CO2” = respiratory component
    • Does the model hold true for all pH values?
      • The Henderson Hasselbach predicts a linear relation between pH and logP CO 2
      B ut in vitro in vivo CO2 equilibration studies demonstrate a non-linear relationship between log PCO2 and pH over a wide range of pH
    • Copyright ©1997 American Physiological Society Constable, P. D. J Appl Physiol 83: 297-311 1997 No Caption Found The curvilinear relationship between pH and log P CO 2
    • Clinical “failures” of the standard model
      • T he mechanism of hyperchloremic acidosis during NaCl administration and cardio-pulmonary bypass *
      • Metabolic alkalosis associated with decreased plasma albumin concentrations **
      ** J Appl Physiol 84: 1740-1748, 1998 * Anesthesiology. 2000 Nov;93(5):1170-3 Anesthesiology 1999, 90:1265--1270 Critical Care 2002, 6(Suppl 2):2
    • New models of acid base balance – the Stewart model
      • They try to offer explanations for such “extreme” phenomena in human physiology and disease
      • Include the “standard” model formulas as special cases
      • Grounded on physical chemistry and equilibrium thermodynamic analysis of uni- and multi-compartmental fluidic systems
        • Can J Physiol Pharmacol 61:1444-1481 1983
        • J Appl Physiol 86:326-334, 1999
        • J Appl Physiol 95:2333-2344, 2003
    • Physico-chemical basis of “new” acid basis models
      • In any physiologic solution, that is at thermodynamic equilibrium the following laws simultaneously apply to all acid/base pairs:
      • Conservation of mass
      • Conservation of charge
      • Law of mass action
    • Acid – base pairs in a physiologic solution
      • Water Dissociation Equilibrium
      • Electrical Neutrality Equation
      • Weak acid (albumin, phosphate, sulfate etc) dissociation equilibrium
      • Conservation of mass for weak acids
      • Bicarbonate ion formation equilibrium (“standard” model)
      • Carbonate ion formation equilibrium
    • Acid – base pairs in a physiologic solution
    • The “modified” Henderson Hasselbach equation
      • Accounting for all these systems simultaneously leads to a modified HH equation:
      K α : dissociation constant for weak acids A tot : total concentration of weak acids SID + : Strong Ion difference = [ Na + ] + [ K + ] – [ Cl - ] – [ lactate ] = [HCO 3 - ]+[A - ]
    • What does this all mean?
      • The bicarbonate acid base system (“standard” HH) is a marker of acid base status (“CXR – pneumonia” concept)
      • The three main “independent” variables that control the pH are:
      • PCO 2 : controlled by the lungs
      • A tot : controlled by the liver
      • SID: kidney, intestine and tissue
    • What does this all mean?
    • Dependent v.s. Independent variables in the Stewart model
      • The designation of certain variables as independent while others (pH) are dependent is a controversial aspect of the theory
      • The theory was developed years before the first epithelial H + transporter was cloned/identified i.e. biological systems do handle protons directly …
    • Dependent v.s. Independent variables II
      • Equilibrium approaches cannot be used to infer causality relations without a model of the system as exists far from equilibrium (ion transport)
      • However equilibrium models render constraints that any quantitative description of the system should obey
      • The modified HH is thus a more general version of the Henderson Hasselbach and include the “6-pack” rule of acid base disorders of the “standard” model
    • Thinking about fluids and RRT in the ICU
      • Even fluids that do not have any CO 2 will have an effect in the pH of body fluids according to the new theory
      • After infusion, the fluid administered will equilibrate with plasma, ECF and finally ECF
      • In the new “equilibrium” state, the SID and A tot of the ECF will change towards the ones of the infused fluid
    • Acid – Base Analysis within the “new” paradigm I
    • Acid – Base Analysis within the “new” paradigm II
    • Clinical Use of the Stewart Model
      • Formulas are more complicated than the standard acid-base approach
      • Calculation of the Strong Ion Difference may be accomplished by the formula:
      Detection of gap acidosis is done by the Strong Ion Gap:
    • Thinking about fluids in the ICU
      • It is the SID value of NS, not the dilution of plasma bicarbonate that causes the “dilutional” acidosis of massive rescuscitation, CPB *
      • Paradoxically, sodium bicarbonate will have an alkalizing effect only if ventilation is not limited (infusion of “high” SID fluid)
      • If ventilation is limited, CO2 will rise, and pH will fall after sodium bicarbonate infusion**
      * Anesth Analg 2003;96:919-922 ** Am. J. Respir. Crit. Care Med., 2000; 161 ( 4 ): 1149-1153 J Nephrol. 2005 18(3):303-7
    • Acid – Base and Chloride Transport I
      • The “independent” variable of SID may explain the following basic science observations:
      • Excretion of any organic anion will decrease SID (Na + will accompany the anion)
      • NH4 + excretion will increase SID (Cl - will accompany the cation but Na + will stay behind)
      • Glimpses of the non-equilibrium model for acid base control might be re-constructed from clinical disorders of ion transport(-ers)
    • Acid – Base and Chloride Transport II
      • A hypochloremic metabolic alkalosis is characteristic of the following disorders:
      • Cystic Fibrosis : due to mutations of CTFR (a chloride channel)
      • Bartter syndrome: due to mutations of ROMK (potassium channel) /NKCC2 (sodium chloride transporter) /CLCNKB (chloride channel)
      • Alkalosis is due to :
      • “ volume contraction” (standard model)
      • elevated SID (Stewart model)
    • Internet Resources
      • UPMC’s Department of Critical Care pHorum (references and excel based calculator of SIG/SID, modified HH):
      • http://www.ccm.upmc.edu/education/resources/phorum.html
      • The full text of Stewart’s 1983 book is available on the web for free: http://www.acidbase.org/
      • A “colorful” introduction at the Anesthetist: http://www.anaesthetist.com/icu/elec/index.htm