This is a quick guide to assessing acid-base disorders using the traditional approach to acid-base analysis. There are many approaches out there. This is one that works for me. Find what works for you, and crack on.
The quick and dirty run through:
Step 1: What’s the pH?
- Normal pH 7.36 – 7.44
- Acidemia pH < 7.36
- Alkalemia pH > 7.44
Step 2: Is the primary problem respiratory, metabolic, or both?
- The respiratory component is determined by assessing the pCO2
- Normal pCO2 is 36-44
- Respiratory acidosis exists if pCO2 > 44
- Respiratory alkalosis exists if pCO2 < 36
- The metabolic component is determined by assessing the bicarbonate
- Normal HCO3 is about 20-22
- Metabolic acidosis exists if HCO3 < 20
- Metabolic alkalosis exists if HCO3 > 22
Notice that when the primary disorder is metabolic the pH and the bicarbonate both move in the same direction – when there is metabolic acidosis both the pH and the bicarbonate go down, and when there is metabolic alkalosis both the pH and the bicarbonate go up. BUT when the primary disorder is respiratory the pH and pCO2 move in opposite directions – when there is respiratory acidosis the pH goes down while the pCO2 goes up, and when there is respiratory alkalosis the pH goes up while the pCO2 goes down.
The easy way to remember which direction the pH will move in relation to the primary disorder is to remember ROME:
RO stands for Respiratory Opposite (when there is a primary respiratory disorder the pH moves one direction and the pCO2 moves the other)
ME stands for Metabolic Equal (when there is a primary metabolic disorder the pH and the bicarbonate both go up or down together)
Step 3: Is compensation occurring?
The body will try to compensate for changes in the pH by adjusting the bicarbonate or pCO2. If the primary problem is metabolic, the body will adjust the rate and depth of respiration to try to move the pH back to a more normal level. Likewise, if the primary problem is respiratory, the body will adjust renal retention or excretion of bicarbonate to try to move the pH back to a more normal level.
The body can adjust the CO2 levels very quickly by changing the respiratory rate and depth, so there is no need to make special adjustments based on how long the metabolic problem has existed. Conversely, it takes time for the body to adjust the pH by altering the excretion or retention of bicarbonate – many hours to days to complete then process – so when we calculate expected compensation for a primary respiratory problem we have to account for how long the problem has existed. The table below can be used to calculate the expected compensation.
There are 2 ‘rules’ about compensation
- The body does NOT overcompensate
- Compensation does NOT return the pH to the normal range
If these rules appear to be broken, then there is a mixed acid-base disturbance, NOT compensation occurring.
Example: a patient has a pH of 7.42, bicarbonate of 11, and pCO2 of 34. Mathematically, this might appear to be a compensated metabolic acidosis. However, the pH has returned to the normal range despite a significant drop in the bicarbonate. It is very likely there is an additional disturbance occurring that needs to be identified and addressed.
Step 4: Evaluate the anion gap if there is metabolic acidosis
- The anion gap is calculated (Na + K) – (Cl – HCO3)
- Normal anion gap for dogs is 8-21
- Normal anion gap for cats is 12-16
Step 5: Determine if other types of metabolic acidosis co-exist with a high anion gap metabolic acidosis
A normal-anion gap acidosis or metabolic alkalosis can co-exist with a HAGMA.
- Calculate the corrected bicarbonate:
- Corrected bicarbonate = measured bicarbonate + anion gap – 14
- Corrected bicarbonate > 22 metabolic alkalosis co-exists
- Corrected bicarbonate < 22 normal anion gap metabolic acidosis co-exists
- Correct for hypoalbuminemia (albumin is an anion):
- For every 1.0g/dL below normal add 2.5 to the anion gap
Step 6: Calculate the osmolality (and osmolar gap if possible)
Most veterinary hospitals do not have the ability to measure the serum osmolality and therefore cannot calculate the osmolar gap.
- Using American Units: Serum osm = 2(Na + K) + (BUN / 2.8) + (Glucose / 18)
- Using SI Units: Serum osm = 2(Na + K) + BUN + Glucose
- Normal calculated serum osm in dogs is about 290mOsm/kg
- Normal calculated serum osm in cats is about 300mOsm/kg
- Osmolar gap = measured serum osm – calculated serum osm
- Normal gap is < 10
- The normal gap exists because the formula for calculated osmolarity does not take into account chloride, phosphate, sulphate, calcium, magnesium, lactate, ammonia, serum proteins, and lipids
Lists of differentials
High anion gap metabolic acidosis (HAGMA)
If there is a high anion gap metabolic acidosis (HAGMA), the differentials can be remembered using the mnemonic GOLD MARK (link to The Lancet editorial discussing why GOLD MARK should replace MUDPILES)
- Glycols (ethylene glycol and propylene glycol)
- Oxoproline (metabolite of acetaminophen, unclear if this is present in significant amounts in dogs and cats)
- Lactate
- D-Lactate (acetaminophen, short bowel syndrome, propylene glycol infusions*)
- Methanol
- Aspirin
- Renal failure
- Ketoacidosis
*In addition to being present in several cleaners, automotive products, and commercial products, propylene glycol is a carrier for many drugs including diazepam and phenobarbital)
Normal anion gap metabolic acidosis (NAGMA)
If there is a normal anion gap metabolic acidosis (NAGMA, also sometimes called hyperchloremic metabolic acidosis) the differentials are things that cause abnormal bicarbonate loss or abnormal chloride retention:
- Drugs
- Acetazolamide
- Acidifying agents
- Cholestyramine
- GI bicarbonate loss
- Diarrhea (common)
- Pancreatic fistula (very rare in veterinary medicine)
- Exogenous chloride administration
- Hypertonic saline
- Large volume ‘normal’ saline
- Renal bicarbonate loss
- Renal tubular acidosis
Causes of a low anion gap (<6)
- Increased unmeasured cations
- Hypercalcemia
- Hypermagnesemia
- Multiple Myeloma
- Decreased unmeasured anions
- Dilution
- Hypoalbuminemia
- Artifact
- Lipemic sample
- Bromide (machine erroneously reads bromide as chloride)
Causes of metabolic alkalosis
- GI loss
- Vomiting
- Pyloric outflow obstructions
- Renal bicarbonate retention
- Hypokalemia
- Hypochloremia
- Chronic hypercapnia
- Urinary acid loss
- Diuretics
- Primary hyperaldosteronism
- Volume contraction/free water loss
- Iatrogenic
- Bicarbonate administration
- Dialysis
Causes of respiratory acidosis
- Airway obstruction
- CNS depression due to drug administration
- Muscular weakness
- Neuromuscular disorders
- Central nervous system lesion (brain or high cervical)
- Lung disease
- Severe pain (holding breath)
Causes of respiratory alkalosis
- Hypoxia-mediated hyperventilation
- Altitude
- Anemia
- V/Q mismatch
- CNS mediated hyperventilation
- Increased intracranial pressure
- Behavioral/psychogenic
- Lesions of the caudal midbrain and pons
- Pulmonary disorders
- Congestive heart failure
- Pneumonia
- Pulmonary embolus
- Mechanical hyperventilation
- Toxin induced
- Nicotine
- Salicylates
- Pain-induced hyperventilation
