Acidosis

Description

• Reduced pH owing to alveolar hypoventilation with elevated PaCO₂
• Defined as PaCO₂ >45 mm Hg or higher than expected for calculated respiratory compensation of a metabolic acidosis
• Divided into 3 broad categories:
  • Primary failure in CNS drive to ventilate:
    • Sleep apnea
    • Anesthesia
    • Sedative overdose
  • Primary failure in transport of CO₂ from alveolar space:
    • COPD
    • Myasthenic crisis
    • Severe hypokalemia
    • Guillain–Barré syndrome
  • Primary failure in transport of CO₂ from tissue to alveoli:
    • Severe heart failure/pulmonary edema

• Reduction in serum pH from decreased plasma [HCO₃^–] or elevated [H⁺] levels
• Primarily caused by:
  • Increased acid formation
  • Decreased acid excretion
  • Loss of bicarbonate
• Metabolic acidosis is clinically evaluated by dividing into 2 main groups:
  • Elevated anion gap metabolic acidosis:
    • Bicarbonate reduced through buffering of added strong acid
    • Anion gap is increased due to retention of the unmeasured anion from the titrated strong acid
  • Normal anion gap metabolic acidosis due to:
    • Kidneys fail to reabsorb or regenerate bicarbonate
    • Losses of bicarbonate from GI tract (diarrhea)
    • Ingestion or infusion of substances that release hydrochloric acid
  • No anion gap is observed owing to the absence of any unmeasured anion of a titrated acid and secondary chloride retention with HCO₃⁻ loss

Etiology

• Respiratory acidosis:
  • Inhibition of respiratory center:
    • Cardiac arrest
    • Drugs (opiates, benzodiazepines, etc.)
    • Meningitis/encephalitis
    • CNS lesions (mass, CVA)
  • Impaired gas exchange:
    • Pulmonary edema
    • Asthma/COPD
    • Pneumonia
    • Interstitial lung disease
    • Obesity
    • Pulmonary contusion
  • Neuromuscular disease:
    • Diaphragmatic paralysis
    • Guillain–Barré syndrome
    • Myasthenia gravis
    • Muscular dystrophy
    • Spinal cord injury
    • Hypokalemia/hypophosphatemia
    • MS
  • Obstructive:
    • Congenital lesions (laryngomalacia)
    • Foreign body aspiration
    • Vascular ring
    • Infectious (epiglottitis, croup, abscess)
• Metabolic acidosis:
  • Anion gap acidosis: Mnemonic A CAT PILES MUD:
    • Alcohol ketoacidosis
    • Carbon monoxide or cyanide
    • Aspirin
    • Toluene
    • Paraldehyde, propylene glycol, phenformin
    • Iron/isoniazid
    • Lactic acidosis
    • Ethylene glycol, ethanol
    • Starvation, salicylates
    • Methanol, metformin
    • Uremia
    • Diabetic ketoacidosis
  • Increased osmolar gap: Mnemonic ME DIE:
    • Methanol
    • Ethylene glycol
    • Diuretics (mannitol; no acidosis)
    • Isopropyl alcohol (no acidosis)
    • Ethanol
  • Nonanion gap metabolic acidosis:
    • GI losses of bicarbonate:
      • Diarrhea (most common cause of nonanion gap metabolic acidosis)
      • Villous adenoma
      • Removal of small bowel, pancreatic, or biliary secretions
      • Tube drainage
      • Small bowel/pancreatic fistula
    • Anion exchange resins (i.e., cholestyramine)
    • Ingestion of calcium chloride or magnesium chloride
    • Type I renal tubular acidosis (distal): Hypokalemic hyperchloremic metabolic acidosis:
      • Decreased ability to secrete hydrogen
      • Serum HCO₃ <15 mEq/L when untreated
      • Potassium low
      • Renal stones common
    • Type II renal tubular acidosis (proximal): Hypokalemic hyperchloremic metabolic acidosis:
      • Decreased proximal reabsorption of HCO₃⁻
      • Acidosis limited by reabsorptive capacity of proximal tubule for HCO₃⁻
      • Serum HCO₃ typically 14–18 mEq/L
      • Low/normal potassium
    • Type IV renal tubular acidosis (hypoaldosteronism): Hyperkalemic hyperchloremic acidosis:
      • Aldosterone deficiency or resistance causing decreased H⁺ secretion
      • Serum bicarb >15 mEq/L
      • Normal/elevated potassium
    • Carbonic anhydrase inhibitors (acetazolamide)
    • Tubulointerstitial renal disease
    • Hypoaldosteronism
    • Hyperalimentation
    • Addition of hydrochloric acid such as:
      • Ammonium chloride
      • Arginine hydrogen chloride
      • Lysine hydrogen chloride

Signs and Symptoms

• Nonspecific findings
• Vital signs:
  • Tachypnea or Kussmaul respirations with metabolic acidosis
  • Hypoventilation with respiratory acidosis
  • Tachycardia
• Somnolence
• Confusion
• Altered mental status (CO₂ narcosis)
• Myocardial conduction and contraction disturbances (dysrhythmias)

Essential Workup

• Electrolytes, BUN, creatinine, and glucose:
  • Decreased bicarbonate with metabolic acidosis
  • Hyperkalemia and hypercalcemia with severe metabolic acidosis
• Arterial blood gases:
  • pH
  • CO₂ retention in respiratory acidosis
  • CO level

• Respiratory acidosis:
  • Acute: Expected HCO₃⁻ increased by 1 mEq/L for every 10 mm Hg increase in PaCO₂
  • Chronic: Expected HCO₃⁻ increased by 4 mEq/L for every 10 mm Hg increase in PaCO₂
• Calculate anion gap: Na⁺ – (HCO₃⁻ + Cl⁻):
  • Correct anion gap for hypoalbuminemia:
    • For every 1 g/dL decrease in albumin (from 4 g/dL), add 2.5 points to calculated anion gap
  • Do not correct sodium concentration when calculating the anion gap in the setting of marked hyperglycemia because hyperglycemia affects the concentration of chloride and bicarbonate, as well as sodium
  • Normal range = 5 – 12 ± 3 mEq/L
  • Anion gap >25 mEq/L is seen only with:
    • Lactic acidosis
    • Ketoacidosis
    • Toxin-associated acidosis
• Calculate the degree of compensation:
  • Expected PaCO₂ = 1.5[HCO₃⁻] + 8
  • If PaCO₂ inappropriately high, patient has a concomitant respiratory acidosis, and/or inadequate compensation
• Evaluate the delta gap (ΔGap):
  • For every 1-point increase in anion gap, HCO₃⁻ should decrease by ∼1 mEq/L in simple acid–base disorder
  • As the volumes of distribution of the unmeasured anions and serum HCO₃⁻ are not in unity, a ΔGap >6 signifies a mixed acid–base disorder
• Evaluate ΔGap by comparing the change in the anion gap (ΔAG) with the change in the HCO₃⁻ (ΔHCO₃⁻) from normal:
  • HCO₃⁻ decrease ≈ AG increase (ΔGap of 0 ± 6) AG acidosis only
  • HCO₃⁻ decrease > AG increase (ΔGap of ≤–6) non-AG metabolic acidosis and respiratory alkalosis
  • HCO₃⁻ decrease < AG increase (ΔGap of ≥6) metabolic alkalosis and respiratory acidosis

Diagnostic Tests and Interpretation

• ABG: See interpretation above
• VBG:
  • Obvious benefit is less patient discomfort and ease in acquiring sample
  • pH varies by <0.04 units when compared to arterial sampling
  • Correlation between venous pCO₂ lacking
  • Limited role in screening for hypercapnia. pCO₂ >45 mm Hg is sensitive (but not specific) for detection of arterial pCO₂ >50 mm Hg in hemodynamically stable patients
  • Useful in simple acid–base disorders
• Urinalysis for glucose and ketones
• Measure serum osmolality:
  • Calculated serum osmolality = 2 Na + glucose/18 + BUN/2.8 +ETOH/4.6
• Osmolar gap = difference between calculated and measured osmolality:
  • Normal = <10
  • Elevated osmolar gap may indicate toxic alcohol as etiology of acidosis
  • Absence of an osmolar gap should never be used to rule out toxic ingestions:
    • Osmolar gap imprecisely defined
    • Delayed presentations may have normal gap
    • Large variance in gap among normal patients
• Toxicology screen:
  • Methanol, ethylene glycol, ethanol, and isopropyl alcohol if increased osmolality gap
  • Aspirin or iron levels for suspected ingestion
• Co-oximetry for CO exposure
• Serum ketones or β-hydroxybutyrate level
• Serum lactate

• May identify cardiomyopathy or CHF
• Underlying pneumonia

• May identify regional wall motion abnormalities or valvular dysfunction
• Evaluate for conduction disturbances

Differential Diagnosis

• Anion gap acidosis:
  • Mnemonic A CATPILES MUD
• Increased osmolar gap:
  • Mnemonic ME DIE

Initial Stabilization/Therapy

• Early intubation for severe metabolic acidosis with progressive/potential weakening of respiratory compensation
• Naloxone, D₅₀W (or POC glucose), and thiamine if mental status altered

Ed Treatment/Procedures

• Respiratory acidosis:
  • Treat underlying disorder
  • Provide ventilatory support for worsening hypercapnia
  • Identify and correct aggravating factors (pneumonia) in chronic hypercapnia
• Metabolic acidosis:
  • Identify if concurrent osmolar gap
  • Treat underlying disorder:
    • Diabetic ketoacidosis
    • Lactic acidosis
    • Alcohol ketoacidosis
    • Ingestion
  • Correct electrolyte abnormalities
• IV fluids:
  • Rehydrate with 0.9% normal saline if patient hypovolemic
  • Consider hemodialysis

Medication

• Dextrose: D₅₀W 1 amp (50 mL or 25 g); (peds: D₂₅W 4 mL/kg) IV
• Naloxone (Narcan): 2 mg (peds: 0.1 mg/kg) IV/IM initial dose
• Thiamine (vitamin B₁): 100 mg (peds: 50 mg) IV/IM

Disposition

• pH <7.1
• Altered mental status
• Respiratory acidosis
• Hemodynamic instability
• Dysrhythmias
• Electrolyte abnormalities

See Also

Alkalosis