BlogBlogMetabolic acidosis

Metabolic acidosis

In this post we simplify the concept of metabolic acidosis and how to tackle in real-world settings.

Diagnosis

  • Metabolic acidosis can only be ruled out if:
    • The anion gap (AG) isn’t elevated (<14).
    •  HCO3 level is normal (22-26).
    • Both have to be present.
  • A normal arterial PH doesn’t rule out metabolic acidosis.
  • A normal serum HCO3 level doesn’t rule out the presence of metabolic acidosis.
  • Elevated AG means elevated AG metabolic acidosis is present regardless of HCO3 level or PH value.
  • Low HCO3 with NAG doesn’t necessarily mean metabolic acidosis as this may represent a compensatory mechanism of respiratory alkalosis.
  • The AG must be calculated on every single BMP or CMP even if HCO3 is normal or even high.

Pathophysiology

Metabolic acidosis:

  •  Due to excess acids in the ECF whether from endogenous production or exogenous consumption (High anion gap)
  • Due to HCO3 loss whether renal or extra-renl (Normal anion gap).

 

Examples:

  • Lactic acidosis (Excess acid due to endogenous acid production) ⇢ High anion gap. acidosis.
  • DKA (Excess acid due to endogenous acid production) ⇢ High anion gap acidosis.
  • Starvation ketosis (Excess acid due to endogenous acid production) ⇢ High anion gap acidosis.
  • Diarrhea ( HCO3 loss)⇢ Normal anion gap acidosis.
  • Diversion of urine into the GI tract ( HCO3 loss)⇢ Normal anion gap acidosis.
  • RTA  ( HCO3 loss)⇢ Normal anion gap acidosis.
  • Saline administration  ( HCO3 loss)⇢ Normal anion gap acidosis.
  • Ethylene glycol consumption (Excess acid due to exogenous acid consumption) ⇢ High anion gap acidosis.
  • Methanol consumption (Excess acid due to exogenous acid consumption) ⇢ High anion gap acidosis.
  • Renal failure:
    • Mild-moderate renal failure ( HCO3 loss)⇢ Normal anion gap acidosis.
    • Advanced renal failure  (Excess acid due to endogenous acid production) ⇢ High anion gap. acidosis.

 

Possible combined disorders

  • AG metabolic acidosis (Excess acids) can be associated with NAG metabolic acidosis (HCO3 loss) or metabolic alkalosis (HCO3 gain):
    • DKA (Excess acid) + Diarrhea (HCO3 loss).
    • Advanced renal failure (Excess acids) + Vomiting (HCO3 absorption).
  • NAG metabolic acidosis and metabolic alkalosis don’t simultaneously coexist:
    • Diarrhea (HCO3 loss) + Vomiting (HCO3 absorption):
      • If the net is HCO3 gain→ Metabolic alkalosis.
      • If the net is HCO3 loss→ NAG metabolic acidosis.

 

To find out if the HAG metabolic acidosis is associated with NAG acidosis or metabolic alkalosis or not, calculate the delta-delta (Δ Δ):

  • First step: calculate the gap between the calculated anion gap and normal anion gap (12).
  • Second step: Add the outcome of the first step to the measured serum bicarb (labeled CO2 on BMP or CMP).
  • Third step: Compare the outcome of the second step to 22:
    • If < 22: there is an associated NAG metabolic acidosis.
    • If 22-26: No associated NAG metabolic acidosis or alkalosis.
    • If > 26: There is an associated metabolic alkalosis.

 

ABG

  • Check the adequacy of respiratory compensation.
  • Confirm a primary respiratory alkalosis if suspected.
  • Assess the severity of acidosis.
  • Always obtain if severe acidosis
  • May not be needed in mild-moderate acidosis.
  • VBG can be used with some adjustments (VBG isn’t reliable to assess hypoxia).

 

Monitoring

  • Most, if not all cases of severe life-threatening acidosis are due to HAG acidosis.
  • NAG acidosis leads to mild-moderate acidosis in most cases.
  • Patients with severe metabolic acidosis should be monitored in the ICU.
  • Be prepared to intubate if inadequate respiratory compensation, altered mental status, or shock.
  • Keep your eyes on the monitor and watch for QRS widening/bradycardia.
  • Closely monitor K and urine output, hyperkalemia can develop quickly, especially in renal failure.
  • Monitor other labs.

 

Treatment

  • Treat the underlying cause that’s leading to acid production and HCO3 loss.

 

HCO3 therapy

HCO3 supplements are effective in treating HCO3 loss (NAG metabolic acidosis) while will help buffer excess acids in HAG acidosis.

 

 

NAG metabolic acidosis:

  • Oral HCO3 in mild-moderate chronic NAG (RTA and CKD).
  • HCO3 drip in severe NAG metabolic acidosis (HCO3 ≤ 15).
  • Replace NS with LR.

 

HAG metabolic acidosis:

  • Push two amps of HCO3 if PH is less than 7.1.
  • The goal is to bring PH ≥ 7.2 or HCO3  ≥ 16.
  • If more HCO3 is required consider starting the HCO3 drip, in life-threatening metabolic acidosis, an effective infusion rate is 250-500 ml/hour (If no fluid overload).

 

HCO3 therapy

  • The Bicarb is mixed in different ratios but the most common one is to mix 8.4 gm in 100 ml of free water which will result in a hypertonic solution with a ratio of 1 ml = 2 meq.
  • The bicarb ampule is a prefilled syringe with 50 cc of NaHCO3 hypertonic solution, each ampule is 100 meq (50 x 2).
  • The Bicarb drip is mixed by diluting 3 amps of NaHCO3 in 1000 ml of free water of D5W, or mixing 1.5 amps in 1000 ml of 045 NS.
  • For NaHCO3 drip to be effective in severe life-threatening metabolic acidosis, it should be infused at a rate of 250-500 ml/hour (if no fluid overload).

 

Hyperkalemia & metabolic acidosis:

  • Metabolic acidosis is associated with hyperkalemia except in RTA 1 & 2, diarrhea, and saline administration.
  • Life-threatening Hyperkalemia may develop quickly in severe acidosis, don’t be deceived by initial normal K, please watch closely and consider aggressive hyperkalemia treatment.
  • Be prepared to push calcium and bicarb and start hemodialysis ( CRRT is way less effective in quick K removal).

 

Acidosis and hypotension

Worsening acidosis may lead to less response to vasopressors leading to worsening hypotension despite more vasopressors, giving HCO3 pushes will improve their BP instantly but temporarily, hyperkalemia is likely present so pushing bicarb and calcium is advisable.

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