References

I 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 Academic
Base 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 - PMC
A 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 Load

Review 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 diet
Not 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 disorders

Introduction to Simple and Mixed Acid-Base Disorders
- Disturbances of acid-base homeostasis are common clinical problems
  - Discussed in Chapters 18-21
  - This chapter reviews:
    - Basic principles of acid-base physiology
    - Mechanisms of abnormalities
    - Evaluation of simple and mixed acid-base disorders
- Acid-Base Physiology
  - Free hydrogen is maintained at a very low concentration
    - 40 nanoEq/L
    - 1 millionth the concentration of Na, K, Cl, HCO3
    - H+ is highly reactive and must be kept at low concentrations
    - Compatible H concentration: 16 to 160 nanoEq/L
      - pH range: 7.8 to 6.8
  - Buffers prevent excessive variation in H concentration
    - Most important buffer: HCO3
    - Reaction: H+ + HCO3 <=> H2CO3 <=> H2O + CO2
      - H2CO3 exists at low concentration compared to its products
    - Henderson-Hasselbalch Equation (HH Equation)
    - Understanding acid-base can use both H+ concentration and pH
- Measurement of pH
  - Must be measured anaerobically to prevent CO2 loss
  - Measurement methods:
    - pH: Electrode permeable to H+
    - PCO2: CO2 electrode
    - HCO3: Calculated using HH Equation
    - Alternative: Add strong acid, measure CO2 released
      - PCO2 * 0.03 gives mEq of CO2
  - Measured vs. Calculated HCO3
    - pKa of 6.1 and PCO2 coefficient (0.03) vary
    - Measurement of CO2 prone to error
    - Debate remains unresolved
    - Differences affect anion gap calculations
  - Arterial vs. Venous Blood Gas (ABG vs. VBG)
    - Venous pH is lower due to CO2 retention
    - Venous blood may be as accurate as arterial for pH if well perfused
  - Pitfalls in pH Measurement
    - Must cool ABG quickly to prevent glycolysis
    - Air bubbles affect gas readings
    - Heparin contamination lowers pH
    - Arterial pH may not reflect tissue pH
      - Reduced pulmonary blood flow skews results
      - End tidal CO2 > 1.5% indicates adequate venous return
- Regulation of Hydrogen Concentration
  - HCO3/CO2 as the Principal Buffer
    - High HCO3 concentration
    - Independent regulation of HCO3 (renal) and PCO2 (lungs)
  - Renal Regulation of HCO3
    - H secretion reabsorbs filtered bicarbonate
    - Loss of HCO3 in urine equates to H retention
    - H combines with NH3 or HPO4, forming new HCO3
  - Pulmonary Regulation of CO2
    - CO2 is not an acid but forms H2CO3
    - Lungs excrete 15,000 mmol of CO2 daily
    - Kidneys excrete 50-100 mmol of H daily
    - H = 24 * (PCO2 / HCO3)
    - pH compensation via respiratory and renal adjustments
Acid-Base Disorders
- Definitions
  - Acidemia: Decreased blood pH
  - Alkalemia: Increased blood pH
  - Acidosis: Process lowering pH
  - Alkalosis: Process raising pH
  - Primary PCO2 abnormalities: Respiratory disorders
  - Primary HCO3 abnormalities: Metabolic disorders
  - Compensation moves in the same direction as the primary disorder
  - Diagnosis requires extracellular pH measurement
- Metabolic Acidosis
  - Low HCO3 and low pH
  - Causes:
    - HCO3 loss (e.g., diarrhea)
    - Buffering of non-carbonic acid (e.g., lactic acid, sulfuric acid in renal failure)
  - Compensation: Increased ventilation lowers PCO2
  - Renal excretion of acid restores pH over days
- Metabolic Alkalosis
  - High HCO3 and high pH
  - Causes:
    - HCO3 administration
    - H loss (e.g., vomiting, diuretics)
  - Compensation: Hypoventilation
  - Renal HCO3 excretion corrects pH unless volume or chloride depleted
- Respiratory Acidosis
  - Due to decreased alveolar ventilation, increasing PCO2
  - Compensation: Increased renal H excretion raises HCO3
    - Acute phase: Large pH drop, small HCO3 increase
    - Chronic phase: Small pH drop, large HCO3 increase
- Respiratory Alkalosis
  - Due to hyperventilation, reducing CO2 and raising pH
  - Compensation: Decreased renal H secretion, leading to bicarbonaturia
  - Time-dependent compensation (acute vs. chronic phases)
- Mixed Acid-Base Disorders
  - Multiple primary disorders can coexist
  - Example:
    - Low arterial pH with:
      - Low HCO3 → Metabolic acidosis
      - High PCO2 → Respiratory acidosis
    - Combination indicates mixed disorder
  - Extent of renal and respiratory compensation clarifies diagnosis
    - Compensation does not fully restore pH
    - Example: pH 7.4, PCO2 60, HCO3 36 → Combined respiratory acidosis & metabolic alkalosis
  - Acid-Base Map illustrates normal responses to disturbances
Clinical Use of Hydrogen Concentration
- H+ vs. pH Relationship
  - H = 24 * (PCO2 / HCO3)
  - Normal HCO3 cancels out 24, so H = 40 nMol/L
  - pH to H conversion:
    - Increase pH by 0.1 → Multiply H by 0.8
    - Decrease pH by 0.1 → Multiply H by 1.25
- Example: Salicylate Toxicity
  - 7.32 / 30 / xx / 15
  - Goal: Alkalinize urine to pH 7.45 (H+ = 35 nMol/L)
  - Bicarb needs to reach 20 for compensation
- Potassium Balance in Acid-Base Disorders
  - Metabolic Acidosis
    - H+ buffered in cells, causing K+ to move extracellularly
    - K+ rises ~0.6 mEq/L per 0.1 pH drop
    - Less predictable in lactic or ketoacidosis
    - DKA-associated hyperkalemia due to insulin deficiency
    - Hyperkalemia can induce mild metabolic acidosis
  - Respiratory Acid-Base Disorders
    - Minimal effect on potassium levels