Blood Gas Analysis
Lori S. Waddell, DVM, DACVECC, University of Pennsylvania
This algorithm reflects canine normals. For cats, substitute feline normals for pH, BE (or HCO3<sup−sup>), PCO2, and PO2 values (Table 1).
Normal Values for Blood Gases
Canine
Feline
Rules of Compensation
Change in respiratory or metabolic component of the acid-base status will normally induce opposite, compensatory change in the other to return the pH toward normal.
Lungs compensate rapidly by changing minute ventilation (respiratory rate/tidal volume/both) within minutes.
Metabolic compensation occurs via the kidneys and is much slower, starting after a few hours and requiring 4 to 5 days for maximum compensation.
Absence or presence and degree of compensation for respiratory disturbance can give an idea of chronicity (Table 2).
Overcompensation does not occur.
If expected compensation is absent, a mixed disturbance is present. For example, if metabolic acidosis is not accompanied by compensatory respiratory alkalosis (the CO2 is normal or increased), a mixed disturbance is occurring with both metabolic acidosis and respiratory acidosis.
Expected Compensatory Changes
BLOOD GAS ANALYSIS ALTERNATIVES
Author Commentary
If blood gas analysis is not available, some information can be obtained through other tests. Pulse oximetry can be used to assess a patient’s oxygenation. It must be remembered that pulse ox saturation and PaO2 are not directly correlated; a pulse ox of 93% corresponds with a PaO2 of 80 mm Hg (10.67 kPa) and a pulse ox of 90% corresponds with a PaO2 of 60 mm Hg (8 kPa). If the patient is intubated, end tidal CO2 (ETCO2) can be used to assess for hypercarbia or hypocarbia. ETCO2 usually corresponds well to the PaCO2, with ETCO2 approximately 5 mm Hg (0.67 kPa) lower than PaCO2 in normal patients. In medium and large dogs, the end tidal tubing can be placed just inside the nostril of an awake, compliant patient to estimate ETCO2.
If anion gap measurement is available on a chemistry screen, it can be used to detect some causes of metabolic acidosis, including those caused by ketones, lactate, and exogenous acids (eg, toxins, phosphates, sulfates). These will all cause an increase in the anion gap. If the anion gap is normal but the corrected chloride is elevated (see equation below), loss of bicarbonate via the kidneys or the large bowel may be causing a metabolic acidosis.
Additionally, the patient’s ketones may be measured via either ketone strips for use with urine or a ketometer to measure serum ketones. A handheld lactate meter can be used to measure ketones. These are relatively inexpensive (typically cost several hundred United States dollars), small pieces of equipment similar to a glucometer and give results in a few minutes. Although they do not give information about pH, they can help guide fluid therapy and potentially help prognosticate in patients that are presented with a high lactate and do not respond to therapy. To detect a metabolic alkalosis, the patient’s chloride concentration should be evaluated. If the corrected chloride is low, a metabolic alkalosis is likely.
Corrected Cl<sup–sup> = (normal Na<sup+sup>/measured Na<sup+sup>) × measured Cl<sup–sup>
This equation helps determine if the chloride concentration is abnormal in comparison to the sodium concentration, as normally the 2 ions will change in the same direction and to the same degree. Changes in the corrected chloride can indicate metabolic derangements.
BE = base excess, HCO3<sup−sup> = bicarbonate, NaHCO3 = sodium bicarbonate, PaCO2 = partial pressure of arterial carbon dioxide, PCO2 = partial pressure carbon dioxide, PO2 = partial pressure oxygen, PPV = positive-pressure ventilation, PvCO2 = partial pressure of venous carbon dioxide