Acidosis, Emergency Medicine

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-Barr © 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-Barr © 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 (Î”Gap):
- 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 Î”Gap > 6 signifies a mixed acid-base disorder
Evaluate Î”Gap by comparing the change in the anion gap (Î”AG) with the change in the HCO3- (Î”HCO3-) from normal:
- If Î”AG > Î”HCO3-, then patient has a concomitant metabolic alkalosis.
- If Î”HCO3- > Î”AG, then patient has concomitant nonanion gap acidosis.

Diagnosis 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
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

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

Follow-Up

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

Failure to appreciate acidosis in mixed acid-base disorders
Failure to appreciate inadequate respiratory compensation for metabolic acidosis and need for ventilatory support
Clues to the presence of a mixed acid-base disorder are normal pH with abnormal PCO2 or HCO3-, when the HCO3- and PCO2 move in opposite directions, or when the pH changes in the direction opposite that expected from a known primary disorder.

Additional Reading

Ayers C, Dixon P. Simple Acid-Base Tutorial. J Parenter Enteral Nutr. 2012;36(1):18-23.
Kellum JA. Determinants of plasma acid-base balance. Crit Care Clin. 2005;21(2):329-346.
Robinson MT, Heffner AC. Acid base disorders. In: Adams J ed. Emergency Medicine. Philadelphia, PA: Elsevier; 2012.
Whittier WL, Rutecki GW. Primer on clinical acid-base problem solving. Dis Mon. 2004;50:122.

Codes

ICD9

276.2 Acidosis

ICD10

E87.2 Acidosis

SNOMED

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

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