Acidosis

[Section Outline]

Description
Etiology

Author:

Matthew T.Robinson

Catherine D.Parker

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 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-Barre syndrome
- Primary failure in transport of CO₂ from tissue to alveoli:
  - Severe heart failure/pulmonary edema

Metabolic acidosis:

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-Barre 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

Diagnosis

⬆ ⬇

[Section Outline]

Signs and Symptoms
Essential Workup
Diagnostic Tests & Interpretation
Differential 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 lab 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:
- 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 & 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 +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

Imaging

CXR:

May identify cardiomyopathy or CHF
Underlying pneumonia

Diagnostic Procedures/Surgery

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

⬆ ⬇

[Section Outline]

Initial Stabilization/Therapy
ED Treatment/Procedures
Medication

Initial Stabilization/Therapy

Airway, breathing, and circulation (ABCs):

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

section name header

Basics ⬇

Diagnosis ⬆ ⬇

Lab

Imaging

Diagnostic Procedures/Surgery

Treatment ⬆ ⬇

Follow-Up ⬆ ⬇

Admission Criteria

Discharge Criteria

Pearls and Pitfalls ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆

Basics

Diagnosis

Treatment

Follow-Up

Pearls and Pitfalls

Additional Reading

Codes