In the past blood gas analysis and interpretation was performed primarily at university and large referral hospitals. The
main argument against not using blood gas analysis to guide case management in private practice was the cost of purchasing
and maintaining a bench-top blood gas analyzer. With the availability of relatively inexpensive point of care units such as
the i-STAT and IRMA, blood gas analysis and interpretation has become more common.
Blood gas analysis begins with collection of the sample. Arterial blood is preferred when assessing respiratory and metabolic
status, but venous blood may be useful for assessment of some metabolic disturbances. The use of free-flowing lingual venous
blood can sometimes be used to estimate arterial blood gas values in anesthetized animals when arterial blood is unobtainable.
The sample should be collected into a heparinized syringe. Usually the syringe is filled with heparin and then emptied. This
process coats the inside of the syringe barrel and the hub of the needle. Alternatively, syringes containing powdered heparin
specifically designed for arterial blood collection are commercially available. Enough blood should be collected (~ 1 ml)
to prevent the heparin from diluting the blood significantly. All visible air should be expelled from the syringe following
sample collection. If the sample is not going to be analyzed immediately it should be capped and placed on ice until it is
Some common errors associated with improper sample collection and storage are:
1. If sample is left uncapped for a prolonged period PaCO2 and PaO2 may be lower. PaO2 may increase if the sample PaO2
is less than the partial pressure of oxygen in room air.
2. If unchilled for a long period cellular metabolism will continue and PaO2 will be lower and PaCO2 increased.
3. If not anticoagulated the sample will cause an error.
Before a blood gas can be interpreted, information about the conditions the animal was exposed to need to be considered. The
fraction of inspired oxygen (FIO2) and body temperature are often required by the blood gas machine for calculation of Alveolar-arterial
(A-a) gradients and temperature corrected values respectively. It is also important to know this information for interpretation
of the blood gas values in the clinical setting.
Many blood gas analyzers measure sodium, potassium, and calcium. Total plasma protein can be measure using a refractometer
or other clinicopathological technique. This additional information will allow calculation of the anion gap or other ionic
differences that can provide insight into the metabolic origin of some acid-base disturbances. These non-traditional approaches
to acid-base balance are not routinely used to manage anesthetic cases intraop. However, these approaches will be encountered
in the context of metabolic acid-base disturbances in Critical Care and Internal Medicine. More information about anion gap
and strong ion difference theory can be found in the recommended reading (1-4).
PaCO2 is the partial pressure of CO2 in the arterial plasma. PaCO2 increases when alveolar minute ventilation is decreased
and vice versa. When PaCO2 increases, ventilation is said to be depressed. Most anesthetic drugs are respiratory depressant
therefore PaCO2 usually is increased from normal during anesthesia unless ventilation is controlled. Carbon dioxide is the
main stimulus for respiration during anesthesia in normal patients.
PaO2 is the partial pressure of oxygen dissolved in the arterial plasma. Alone, this value does not tell you how much oxygen
is in the blood. Hemoglobin is the major carrier of oxygen in blood, NOT dissolved oxygen in plasma; therefore hematocrit
or hemoglobin concentration is also required before estimating oxygen content. The relationship between the PO2 and O2 content
is estimated by the equation:
Oxygen Content (ml/dL)=(Hemoglobin conc. (g/dL) x %hemoglobin saturation x 1.3) + 0.003 x PaO2
The value of 1.3 used in this equation is commonly given as a constant but it is variable between species. This equation calculates
the amount of oxygen carried by the hemoglobin (Hemoglobin conc. (g/dL) x % hemoglobin saturation) and the amount carried
as dissolved oxygen in the plasma water (0.003 x PaO2). Anemic animals may have high PaO2 values but have very little O2 content
(capacity) because hemoglobin concentration is reduced. Hemoglobin saturation measured from an arterial blood sample (SaO2)
is a calculated value based on the oxyhemoglobin dissociation curve. Alternatively, hemoglobin saturation can be measured
with a pulse oximeter (SpO2) and PaO2 estimated without analyzing a blood gas. Normal PaO2 values will vary with FIO2 and
can be calculated using the alveolar gas equation. However, an estimate can be quickly made by multiplying the % inspired
oxygen by 5. For example, when breathing room air (21% O2) a normal PaO2 should be around 100 mmHg. When on 100% oxygen it
should be closer to 500 mmHg. Hypoxemia (i.e., low PaO2) becomes a critical concern demanding immediate attention in most
anesthetized animals when it falls below 60 mmHg because SaO2 and oxygen content fall precipitously below this PaO2 value.
Bicarbonate concentration is calculated from the PaCO2 value using a mathematical relationship programmed into the analyzer.
Actual and standardized values are reported by some machines. Standardized values are corrected to 37 degrees Celsius, a PaCO2
of 40 mmHg, and normal oxygenation.
Total CO2 is given, but the total CO2 in the blood is largely a function of the actual bicarbonate concentration. Usually
95% of the total CO2 reported is due to the actual bicarbonate concentration. It is not an independent measure of acid-base
status because it depends on actual bicarbonate, which in turn depends on PaCO2.
Base excess (BE) is the amount of strong acid needed to titrate the pH of 100% oxygenated human blood to 7.4 at 37 degrees
Celsius and at a PaCO2 of 40 mmHg. This parameter is often referred to as a base deficit, but is also frequently called negative
base excess. Normal BE for a human is 0 +/- 2, but veterinary patients will vary more depending on species. Base excess is
influenced by the total serum protein concentration and will decrease approximately 2.9 mEq/L for every 1 g/dL increase in
total protein. Base excess gives an indication of the metabolic component of acid-base disturbances and is generally unaffected
by changes in PaCO2. Base excess values can be used to calculate a replacement bicarbonate dose when used to correct a "metabolic"
acidosis. The formula is usually given as: Body Weight (in kg) x BE x 0.3 (or some other factor). The factor 0.3 is used for
acute corrections because bicarbonate distributes to the extracellular fluid acutely. When chronic bicarb therapy is indicated,
other factors such as 0.6, are sometimes used because usually bicarbonate therapy is targeted to the total body water (a larger
volume of distribution). During anesthesia we are correcting acutely so 0.3 is most commonly used. A word of caution: when
giving bicarbonate to patients, it is often administered slowly and only 25-33% of the calculated amount is given in any one
dose. This is because when acids are neutralized by bicarbonate, CO2 is rapidly produced. This CO2 must be removed (usually
by the lung) otherwise severe hypercapnea and paradoxical cerebral acidosis may result. Under anesthesia some degree of respiratory
depression is usually present and the patient will not be able to excrete large amounts of CO2 as efficiently as conscious
The Alveolar-arterial oxygen difference (AaDO2 or A-a gradient) is an indication of the difference in oxygen partial pressure
between the gas in the alveoli and the blood leaving the left ventricle (assumed to be the same as the blood in the pulmonary
capillaries). The a/A ratio is a different calculation that provides the same information.