Acid Base Disorders


  • Acidemia: Arterial blood pH below the normal range (<7.36)
  • Alkalemia: Arterial blood pH above the normal range (>7.44)
  • Acidosis: a process that tends to lower the pH (can be caused by fall in serum bicarbonate or a rise in PCO2
  • Alkalosis: a process that tends to raise the pH (can be caused by increase in serum bicarbonate or a decrease in PCO2
  • Base Excess: the amount of strong acid needed to bring a solution back to a pH of 7.4 while keeping PCO2 at 40 mmHg
  • Anion gap: A calculated value that indicates the presence of typically unmeasured anions (AG= Na -Cl -HCO3) with normal values ~8-12 mEq/L, primarily reflecting the presence of unmeasured organic acids
  • Corrected anion gap: Albumin is negatively charged, effectively an "anion." In cases of hypoalbuminemia, Cl and HCO3 must increase to maintain electroneutrality. Hence, the AG will be falsely low as a result of hypoalbuminemia. Thus, you can correct for this: AGcorr=AG + 2.5 (normal albumin of 4 g/dl - measured albumin g/dl)

Normal values

  • Arterial samples: pH 7.36-7.44, HCO3 21-27, PCO2 36-44
  • Venous: pH 0.03 units lower, HCO3 similar, PCO2 3-8 higher
  • Capillary: similar to arterial (assuming no prolonged tourniquet use, ischemia, etc)

General Approach to Diagnosis

1. Look at the pH. What is the primary process occurring? 
  • low pH and high PCO2: respiratory acidosis
  • high pH and low PCO2: respiratory alkalosis
  • low pH and low HCO3: metabolic acidosis
  • high pH and high HCO3: metabolic alkalosis
  • if the pH is near normal but PCO2 and HCO3 are significantly abnormal, there is likely a mixed disorder
2. Assess the degree/chronicity of compensation present. 
  • Acute respiratory acidosis: HCO3 increases by 1 me/L and pH decreased by 0.08 for every 10 mmHg increase in PCO2
  • Chronic respiratory acidosis (3-5 days for renal compensation): HCO3 increases by 4me/L for and pH decreased by 0.03 for every 10 mmHg increase in PCO2
  • Metabolic acidosis: Expected PCO2= 1.5 X HCO3 + 8 +/-2 (Winter's Formula) or the decimal digits of pH should be similar to the PCO2 (ie pH 7.25 should have a PCO2 of 25 in a metabolic acidosis). If the patient's PCO2 is higher than expected, there is a concurrent respiratory acidosis. If the patient's PCO2 is lower than expected, there is a concurrent respiratory alkalosis. If it similar to expected, the compensation is appropriate
  • Metabolic alkalosis: PCO2 increases by 0.7 mmHg for every 1 meq/L increase in HCO3
3. If there is a metabolic acidosis, assess the anion gap. 
  • Elevated anion gap --> MUDPILES (Methanol, uremia, diabetic ketoacidosis, propylene glycol, INH, lactic acidosis, ethylene glycol, salicylates)
    • If there is an elevated anion gap, consider calculating the ∆/∆ = ∆ Anion gap/∆ [HCO3-]. <0.4 is consistent with hyperchloremic nongap acidosis, <1 with high AG and normal AG acidosis, 1-2 pure AG acidosis, >2 concurrent metabolic alkalosis or preexisting compensated respiratory acidosis
  • Normal anion gap--> Bicarbonate loss (ie diarrhea, renal tubular acidosis) or increased chloride (ie normal saline fluid resuscitation leading to hyperchloremia)

                                                                                                From Berend et al, NEJM 2014


Treatment involves addressing the underlying cause as while extreme alterations in pH can potentially cause cellular and protein dysfunction (ie myocardial depression), it is critical to address the underlying cause to ultimately correct the derangement.

  • Respiratory alkalosis: Correct underlying cause (turn down ventilator rate or volume if iatrogenic, treat pain, correct hyperammonemia, etc)
  • Metabolic acidosis: Correct underlying cause (DKA, impaired tissue perfusion and oxygenation or hepatic failure with lactic acidosis, renal failure, reduce chloride load, etc)
    • Sodium bicarbonate: While useful in nongap acidosis, sodium bicarbonate may actually be detrimental in lactic and diabetic ketoacidosis (can paradoxically decrease intracellular pH due to the dissociation into CO2 and H2O and rapid distribution of CO2 across cell membranes). While very low pH levels can potentially lead to myocardial depression, some studies suggest that bicarbonate therapy is no better than saline in improving hemodynamics. Hence, its use in metabolic acidosis should be limited to specific indications such as with hyperkalemia, TCA overdose, ASA ingestion, or potentially with very severe decreases in pH (no certainty of a cutoff value although current Surviving Sepsis Guidelines suggest not using bicarbonate with pH >7.15). In addition, because bicarbonate readily dissociates into CO2 and H2O, in patients with impaired ventilation, it can actually worsen the acidosis
    • THAM: Tris(hydroxymethyl)aminomethane is an amino alcohol that as a weak base, serves as a buffer. Unlike bicarbonate, it does not dissociate into CO2 and thus would not worsen acidosis in a patient with impaired ventilation. There is alack of data regarding its efficacy and thus its use is fairly limited. Dosing (cc of 0.3M) = kg x base deficit x 1.1
    • Dialysis: Can be used to obtain metabolic control and normalize pH. Its use for lactate clearance is not clear as kinetic studies do not suggest removal can counteract lactate production in any meaningful way
  • Metabolic alkalosis: Treat underlying cause (vomiting or gastric drainage, diuretic use, hyperaldosteronism, etc). One can also use acidifying agents such as acetazolamide or ammonium chloride to counteract iatrogenic metabolic alkalosis (ie from prolonged diuretic administration)