Acidosis

Basics

Description

Respiratory acidosis.
  • Reduced pH owing to alveolar hypoventilation with elevated PaCO2
  • Defined as PaCO2 >45 mm Hg or higher than expected for calculated respiratory compensation for 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
Metabolic acidosis
  • Process that reduces serum pH by decreasing plasma bicarbonate levels
  • Primarily caused by:
    • Accumulation of a strong acid through ingestion or metabolism
    • Loss of bicarbonate from the body
  • 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)
  • Anion gap acidosis: Mnemonic A CAT PILES MUD:
    • Alcohol ketoacidosis
    • Carbon monoxide or cyanide
    • Aspirin
    • Toluene
    • Paraldehyde
    • Iron/isoniazid
    • Lactic acidosis
    • Ethylene glycol
    • Starvation
    • Methanol
    • 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
      • 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
    • Tubulointerstitial renal disease
    • Hypoaldosteronism
    • Addition of hydrochloric acid such as:
      • Ammonium chloride
      • Arginine hydrogen chloride
      • Lysine hydrogen chloride

Diagnosis

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
Check the degree of compensation by calculating the expected values and comparing them to the observed laboratory values as follows:
  • 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:
    • If ΔAG > ΔHCO3−, then patient has a concomitant metabolic alkalosis.
    • If ΔHCO3− > ΔAG, then patient has concomitant nonanion gap acidosis.

Diagnostic Tests and Interpretation

Lab
  • 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
  • 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

Imaging
CXR:
  • May identify cardiomyopathy or CHF
  • Underlying pneumonia

Diagnostic Procedures/Other
ECG:
  • 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

Treatment

Initial Stabilization/Therapy

Airway, breathing, and circulation (ABCs):
  • Early intubation for severe metabolic acidosis with progressive/potential weakening of respiratory compensation
  • Naloxone, D50W (or Accu-Chek), 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 or IM initial dose
  • Thiamine (vitamin B1): 100 mg (peds: 50 mg) IV or IM

Ongoing Care

Disposition

Admission Criteria
Consider ICU admission if:
  • pH <7.1
  • Altered mental status
  • Respiratory acidosis
  • Hemodynamic instability
  • Dysrhythmias
  • Electrolyte abnormalities

Discharge Criteria
Resolving or resolved anion gap metabolic acidosis

Pearls and Pitfalls

Additional Reading


See Also

Alkalosis

Codes

ICD-9

276.2 Acidosis

ICD-10

Acidosis

SNOMED

  • 51387008 Acidosis (disorder)
  • 12326000 Respiratory acidosis (disorder)
  • 59455009 Metabolic acidosis (disorder)

Authors

Matthew T. Robinson


© Wolters Kluwer Health Lippincott Williams & Wilkins

Acidosis is a sample topic from the 5-Minute Emergency Consult.

To view other topics, please or .

Emergency Central is a collection of disease, drug, and test information including 5-Minute Emergency Medicine Consult, Davis’s Drug, McGraw-Hill Medical’s Diagnosaurus®, Pocket Guide to Diagnostic Tests, and MEDLINE Journals created for emergency medicine professionals. .