Acid-Base

Ned Hardison, Trey Richardson

Acid base background

  • Abnormal serum H+ concentrations lead to impaired cellular function (cardiac arrest, vasodilation, decreased response to catecholamines), electrolyte abnormalities (e.g. hypo- and hyperkalemia, hypo- and hypercalcemia), impaired glucose metabolism, impaired drug metabolism, and other complications that translate to increased morbidity and mortality
  • ABG/VBG reference range
    • pH = 7.36-7.44 (~7.32-7.40)
    • PCO2 = 36-44 mmHg
    • pO2: 60-100 mmHg
    • HCO3 = 22-26 mEq/L
  • Useful formulas
    • pH on ABG = VBG pH + 0.035
    • Anion Gap= Na-(Cl+Bicarb), normal = 12-14
    • Calculated Osmolarity= 2[Na]+ ([Glucose]/18) + ([BUN]/2.8)
    • Osmolar gap= Measured osmolarity
    • Calculated osmolarity
    • Winter’s formula for respiratory compensation for AGMA: expected pCO2 = 1.5 (serum bicarb) +8 ± 2
      • Shortcut: Expected pCO2 = last two digits of pH

General approach to acid-base derangements

  • Step 1: Determine if the patient is acidemic or alkalemic (look at the pH)
  • Step 2: Determine the primary disorder (metabolic or respiratory)
  • Step 3: Calculate anion gap (see section below)
  • Step 4: Is there appropriate compensation?
  • Step 5: Evaluate for secondary disorders

Anion gap metabolic acidosis (AGMA)

Background

  • Na+ is the predominant cation in normal plasma. Cl- and HCO3- are the predominant anions. There are anions that are not directly measured (e.g. most binding globulins, immunoglobulins, clotting factors, and other proteins). These unmeasured anions are responsible for the normal anion gap of ~12 meq/L. When there are extra unmeasured anions within the plasma, the anion gap increases.

Differential

  • GOLDMARK: Glycols, oxyproline (acetaminophen metabolite), L-lactate, D-lactate, methanol, ASA, renal failure/uremia, ketoacids

Evaluate for secondary disorders

  • Corrected bicarbonate
    • Corrected HCO3 = patient’s HCO3 + (patient’s anion gap - 12)
      • Corrected HCO3 > 26, coexisting metabolic alkalosis,
      • Corrected HCO3 < 22 coexisting non-AG metabolic acidosis

Osmolar gap

  • If there is an anion gap, it is worthwhile to always calculate an osmolar gap. You will be surprised the number of toxic ingestions you catch this way

Non-anion gap metabolic acidosis (NAGMA)

Differential

  • HARDUP: hyperalimentation (starting TPN), acetazolamide use, RTA, diarrhea, uretosigmoid fistula, pancreatic fistula
  • There are two places from which people can waste bicarbonate- the kidneys and the gut
    • The urine anion-gap, which corresponds to unmeasured urinary NH4+ (primary means of renal acid excretion), can differentiate between the two.
    • Urine anion gap (only useful In setting of NAGMA) = Unmeasured cations (NH4+) – unmeasured anions = UNa + UK – UCl
      • Positive value low ° NH4+ ° renal losses
      • RTA
      • Carbonic anhydrase inhibition: acetazolamide, topiramate
      • Adrenal insufficiency
      • Normal saline infusion
  • Ne-GUT-ive value ° high NH4+ ° kidneys working appropriately ° GI losses
    • Diarrhea
    • Pancreatic fistula
    • Ureterosigmoidostomy
  • Caveat: Proximal RTA has a normal distal urine acidification and has a negative urine AG

Managing metabolic acidosis

  • Lactic acidosis is the most common cause AGMA that we encounter
  • In general, avoid use of bicarbonate to treat lactic acidosis
    • Remember: H+ + HCO3- <-> H2CO3 <-> H2O + CO2. While administering bicarbonate will transiently improve pH, carbonic acid will eventually form and ultimately worsen acidemia
  • In acute NAGMA, reasonable to give bicarbonate when bicarb <12 or pH <7.1-7.2
    • Pay close attention to other electrolyte levels, especially K+ as it shifts back into cells

Metabolic alkalosis

Background

  • Metabolic alkalosis occurs as a primary disorder or as compensation for respiratory acidosis. A thorough history and exam can usually clarify which of these two scenarios is occurring
  • In order for metabolic alkalosis to occur, there has to be both an inciting phase (e.g. volume depletion) and a maintenance phase (e.g. hypochloremia or hypokalemia)

Presentation

  • Most symptoms of metabolic alkalosis (confusion, nausea, vomiting, tremors) occur as a result of other electrolyte abnormalities (hypocalcemia, hypokalemia)
  • Serum pH of >7.55 is likely the threshold where symptoms will develop

Causes

  • Saline responsive (e.g. hypochloremia)
    • True volume depletion
    • NG suction/nausea/vomiting
    • Diuretic use
  • Saline refractory
    • Hypokalemia
    • Milk-alkali syndrome
    • Mineralocorticoid excess states
    • Bartters syndrome
    • Gitelman’s syndrome

Treatment

  • Saline responsive/hypochloremia
    • If volume deplete, then normal saline is treatment of choice
    • If alkalosis develops in setting of diuresis, then make sure replacing KCl and consider acetazolamide
  • Saline refractory
    • Hypokalemia: replenish potassium stores
    • Hyperaldosteronism: see Endocrinology section for more detail
    • Bartter syndrome and Gitelman syndrome: replace electrolytes and refer to Nephrology
Last updated on