Chapter Seventeen: Introduction to Simple and Mixed Acid-Base Disorders

ReferencesI said I used MDCalc but I was mistaken I use MedCalX which is nice but getting dated. We talked about this out of print book that we love: Cohen, J. J., Kassirer, J. P. (1982). Acid-base. United States: Little, Brown.Josh mentioned this article that looked at over 17,000 samples with simultaneous measured and calculated bicarbonate and found a very small difference. Comparison of Measured and Calculated Bicarbonate Values | Clinical Chemistry | Oxford AcademicBase deficit or excess- Diagnostic Use of Base Excess in Acid–Base Disorders | NEJM (check out the accompanying letter to the editor from Melanie challenging this article! Along with colleagues Lecker and Zeidel Diagnostic Use of Base Excess in Acid-Base Disorders )Melanie loves this paper which shows a nice correlation between arterial and venous pH but the rest of the comparisons are disappointing - Comparison of arterial and venous pH, bicarbonate, Pco2 and Po2 in initial emergency department assessment - PMCA nomogram for the interpretation of acid-base data is figure 17-1 in the book, this manuscript with the ! in the conclusion creates the acid-base map. We debated about whether we like Winter’s formula: Quantitative displacement of acid-base equilibrium in metabolic acidosis (melanie does b/c it used real patients). Amy’s Voice of God on Dietary Acid LoadReview of dietary acid load: https://pubmed.ncbi.nlm.nih.gov/23439373/, https://pubmed.ncbi.nlm.nih.gov/38282081/, https://pubmed.ncbi.nlm.nih.gov/33075387/Survey data from kidney stone formers regarding sources of dietary acid load: https://pubmed.ncbi.nlm.nih.gov/35752401/Urine profile for vegans and omnivories (urine pH and cations/anions): https://pubmed.ncbi.nlm.nih.gov/36364731/SWAP-MEAT pilot trial: https://pubmed.ncbi.nlm.nih.gov/39514692/ looked at urine profile on plant based meat diet (Beyond Meat) versus animal based meat dietNot all plant meat substitutes are the same in terms of net acid load: https://pubmed.ncbi.nlm.nih.gov/38504022/Frassetto paper showing that the dietary acid load effect is mostly from sodium chloride: https://pubmed.ncbi.nlm.nih.gov/17522265/Healthy eating is probably more important than plant based diet for CKD: https://pubmed.ncbi.nlm.nih.gov/37648119/, https://pubmed.ncbi.nlm.nih.gov/32268544/KDIGO 2024 guidelines: https://kdigo.org/guidelines/ckd-evaluation-and-management/Association (or lack thereof) of a pro-vegetarian diet and sarcopenia/protein energy wasting in CKD: https://pubmed.ncbi.nlm.nih.gov/39085942/Outline Chapter 17 Introduction to simple and mixed acid-base disordersIntroduction to Simple and Mixed Acid-Base DisordersDisturbances of acid-base homeostasis are common clinical problemsDiscussed in Chapters 18-21This chapter reviews:Basic principles of acid-base physiologyMechanisms of abnormalitiesEvaluation of simple and mixed acid-base disordersAcid-Base PhysiologyFree hydrogen is maintained at a very low concentration40 nanoEq/L1 millionth the concentration of Na, K, Cl, HCO3H+ is highly reactive and must be kept at low concentrationsCompatible H concentration: 16 to 160 nanoEq/LpH range: 7.8 to 6.8Buffers prevent excessive variation in H concentrationMost important buffer: HCO3Reaction: H+ + HCO3 <=> H2CO3 <=> H2O + CO2H2CO3 exists at low concentration compared to its productsHenderson-Hasselbalch Equation (HH Equation)Understanding acid-base can use both H+ concentration and pHMeasurement of pHMust be measured anaerobically to prevent CO2 lossMeasurement methods:pH: Electrode permeable to H+PCO2: CO2 electrodeHCO3: Calculated using HH EquationAlternative: Add strong acid, measure CO2 releasedPCO2 * 0.03 gives mEq of CO2Measured vs. Calculated HCO3pKa of 6.1 and PCO2 coefficient (0.03) varyMeasurement of CO2 prone to errorDebate remains unresolvedDifferences affect anion gap calculationsArterial vs. Venous Blood Gas (ABG vs. VBG)Venous pH is lower due to CO2 retentionVenous blood may be as accurate as arterial for pH if well perfusedPitfalls in pH MeasurementMust cool ABG quickly to prevent glycolysisAir bubbles affect gas readingsHeparin contamination lowers pHArterial pH may not reflect tissue pHReduced pulmonary blood flow skews resultsEnd tidal CO2 > 1.5% indicates adequate venous returnRegulation of Hydrogen ConcentrationHCO3/CO2 as the Principal BufferHigh HCO3 concentrationIndependent regulation of HCO3 (renal) and PCO2 (lungs)Renal Regulation of HCO3H secretion reabsorbs filtered bicarbonateLoss of HCO3 in urine equates to H retentionH combines with NH3 or HPO4, forming new HCO3Pulmonary Regulation of CO2CO2 is not an acid but forms H2CO3Lungs excrete 15,000 mmol of CO2 dailyKidneys excrete 50-100 mmol of H dailyH = 24 * (PCO2 / HCO3)pH compensation via respiratory and renal adjustmentsAcid-Base DisordersDefinitionsAcidemia: Decreased blood pHAlkalemia: Increased blood pHAcidosis: Process lowering pHAlkalosis: Process raising pHPrimary PCO2 abnormalities: Respiratory disordersPrimary HCO3 abnormalities: Metabolic disordersCompensation moves in the same direction as the primary disorderDiagnosis requires extracellular pH measurementMetabolic AcidosisLow HCO3 and low pHCauses:HCO3 loss (e.g., diarrhea)Buffering of non-carbonic acid (e.g., lactic acid, sulfuric acid in renal failure)Compensation: Increased ventilation lowers PCO2Renal excretion of acid restores pH over daysMetabolic AlkalosisHigh HCO3 and high pHCauses:HCO3 administrationH loss (e.g., vomiting, diuretics)Compensation: HypoventilationRenal HCO3 excretion corrects pH unless volume or chloride depletedRespiratory AcidosisDue to decreased alveolar ventilation, increasing PCO2Compensation: Increased renal H excretion raises HCO3Acute phase: Large pH drop, small HCO3 increaseChronic phase: Small pH drop, large HCO3 increaseRespiratory AlkalosisDue to hyperventilation, reducing CO2 and raising pHCompensation: Decreased renal H secretion, leading to bicarbonaturiaTime-dependent compensation (acute vs. chronic phases)Mixed Acid-Base DisordersMultiple primary disorders can coexistExample:Low arterial pH with:Low HCO3 → Metabolic acidosisHigh PCO2 → Respiratory acidosisCombination indicates mixed disorderExtent of renal and respiratory compensation clarifies diagnosisCompensation does not fully restore pHExample: pH 7.4, PCO2 60, HCO3 36 → Combined respiratory acidosis & metabolic alkalosisAcid-Base Map illustrates normal responses to disturbancesClinical Use of Hydrogen ConcentrationH+ vs. pH RelationshipH = 24 * (PCO2 / HCO3)Normal HCO3 cancels out 24, so H = 40 nMol/LpH to H conversion:Increase pH by 0.1 → Multiply H by 0.8Decrease pH by 0.1 → Multiply H by 1.25Example: Salicylate Toxicity7.32 / 30 / xx / 15Goal: Alkalinize urine to pH 7.45 (H+ = 35 nMol/L)Bicarb needs to reach 20 for compensationPotassium Balance in Acid-Base DisordersMetabolic AcidosisH+ buffered in cells, causing K+ to move extracellularlyK+ rises ~0.6 mEq/L per 0.1 pH dropLess predictable in lactic or ketoacidosisDKA-associated hyperkalemia due to insulin deficiencyHyperkalemia can induce mild metabolic acidosisRespiratory Acid-Base DisordersMinimal effect on potassium levels