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:
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
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:
- Increased osmolar gap:
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
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
- AntonogiannakiEM, MitrouskaI, AmargianitakisV, et al. Evaluation of acid-base status in patients admitted to ED-physicochemical vs traditional approaches . Am J Emer Med. 2015;33(3):378-382.
- RiceM, IsmailB, PillowMT. Approach to metabolic acidosis in the emergency department . Emerg Med Clin North Am. 2014;32(2):403-420.
- WienerSW. Toxicologic acid-base disorders . Emerg Med Clin North Am. 2014;32(1):149-165.
See Also (Topic, Algorithm, Electronic Media Element)
Alkalosis