Arterial blood gas analysis and interpretation in small animal practice (Proceedings)


In the past blood gas analysis and interpretation was performed primarily at university and large referral hospitals.

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 run.

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.

Analyzer Outputs

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 animals.

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.

Simplified Approach to Blood Gas Interpretation

An arterial blood gas analysis will provide 2 separate, but related pieces of clinical information. First it gives the clinician information on the acid-base status of the patient (pH, HCO3-, BE). Secondly, it provides information on the respiratory status of the patient (PaO2, PaCO2, A-a).

Respiratory Status

Oxygen is less diffusible than CO2 so impairments to diffusion will cause the A-a difference to increase. A more common cause of increased AaDO2 during anesthesia is mixing of non-oxygenated blood with oxygenated blood (e.g., shunting or V/Q mismatch). Unoxygenated hemoglobin will mix with oxygenated hemoglobin and "steal" oxygen away until both are equally saturated. Due to the shape of the oxyhemoglobin dissociation curve the PO2 will not directly tell you the magnitude of the arterial-venous mixing. Normal A-a gradients are generally lower than 25 mmHg on room air (FIO2 ~ 0.21) but may increase at higher FIO2 values. During anesthesia it is very common to have increased V/Q mismatch and A-a gradients, especially in large animals.

Carbon dioxide production is usually relatively constant during anesthesia. Since the majority of CO2 produced is excreted through the lungs, changes in minute ventilation will alter measured PaCO2 (increased minute ventilation will decrease PaCO2 and vice versa). When minute ventilation is doubled, PaCO2 will decrease by approximately 50%. When minute ventilation is halved, PaCO2 will approximately double. This relationship is worthwhile knowing because it allows an anesthetist to adjust a ventilator to maintain a desired PaCO2 during anesthesia.

Acid-Base Interpretation

The following approach can be used to quickly assess acid-base status of patients during anesthesia. Please appreciate there are other less traditional methods that are better suited to characterize metabolic disturbances. These include the Strong Ion Model and Simplified Strong Ion Model. These methods may be more appropriate for acid-base assessment of patients with metabolic disturbances such as lactic acidosis or renal disease. Metabolic disturbances usually are more chronic and complex than anesthesia-induced respiratory disturbances. These acid-base disturbances are often corrected before, or are tolerated during, anesthesia. It may be less problematic to correct chronic abnormalities slowly rather than correcting them during a short anesthetic-surgical procedure. Acute respiratory depression and/or hypoxia are common during anesthesia and are usually corrected rapidly.

The traditional approach to assessing acid-base disturbances is based on the Hendersson-Hasselbalch equation. pH is used as a measure of overall acid-base status, PaCO2 is an independent measure of the respiratory component of acid-base balance, while extracellular base excess (BE) is an independent measure of the nonrespiratory (metabolic) component of acid-base balance. Four primary disturbances are possible:

respiratory acidosis- increased CO2

respiratory alkalosis- decreased CO2

metabolic acidosis- decreased base excess

metabolic alkalosis- increased base excess

Compensation may occur to reduce the magnitude of the primary abnormality, but never results in over-correction.

The first step to interpretation is determination of the primary disturbance. The pH indicates the direction of the primary condition (e.g., if pH decreases the primary condition is causing acidosis or if it increases the primary condition is causing alkalosis).

The second step is to determine if the primary condition has a respiratory component. If the primary condition is acidosis with a respiratory component the PaCO2 should increase. If PaCO2 were decreased it would be concluded that there is respiratory compensation (can be partial or complete depending on the duration of the condition). Compensation takes some time and may not be obvious if the sample is collected early in the acid-base derangement. If the primary condition is an alkalosis with a respiratory component the PaCO2 should be decreased. If PaCO2 is increased this indicates respiratory compensation.

The next step is to determine if the primary condition has a metabolic component. If the primary condition is an acidosis with a metabolic component the BE should be decreased. If it were increased there would be metabolic compensation. Conversely, if the primary disturbance is an alkalosis with a metabolic component then the BE should be increased. A BE decrease would indicated there is metabolic compensation. Again sufficient time is necessary for compensation to occur.

Some patients have mixed acid-base disturbances, that is, they have 2 or more simultaneous respiratory and/or metabolic conditions associated with the primary disturbance (e.g., a simultaneous respiratory acidosis and metabolic acidosis). This is particularly common during anesthesia when the patient has a preexisting metabolic acidosis. When the patient is anesthetized and respiratory depression occurs, the PaCO2 will increase and any respiratory compensation that had occurred will be replaced by a respiratory acidosis. Patients may also have 2 or more different metabolic diseases occurring simultaneously. An example of 2 metabolic diseases would be diabetic ketoacidosis with a superimposed lactic acidosis. Another possible condition is the presence of two or more disorders that may have opposite effects on pH (offsetting), resulting in a reduction in the magnitude of the primary disturbance.

Acid-base disturbances are not primary diseases, but rather are symptoms of an underlying condition that should be diagnosed and corrected. For example, treating an acidosis with bicarbonate (or with another alkalinizing agent) without treating the underlying cause will only mask the clinical signs and may not improve patient survival. Likewise, treating a respiratory acidosis with an alkalinizing agent is contraindicated! The correct treatment for a respiratory acidosis is increasing ventilation. Addition of bicarbonate will only worsen hypercarbia if ventilation cannot compensate. When a primary metabolic disturbance occurs it is often worthwhile to analyze the blood gas with non-traditional methods and interpret the results in the context of the clinical picture.

The influence of plasma constituents on the apparent acid-base balance of the patient should be understood. This cannot be adequately addressed in one lecture, but appreciate common protein, bicarbonate, and electrolyte changes can cause alterations in the patient's overall acid-base status. For example, dilutional acidosis can occur following volume expansion of the extracellular fluid by a alkali-free chloride containing solution (0.9% NaCl). This occurs because HCO3- is decreased due to the rapid absorption of Cl- in the kidney. A solution containing less chloride (0.45% NaCl) would reduce this effect. The opposite occurs when free water is lost and the extracellular fluid constituents are concentrated. In this instance sodium is often elevated producing a hypernatremic or contraction alkalosis. Following severe diarrhea bicarbonate is lost in excess of Cl- leading to a hyperchloremic acidosis. This may be confounded further by a lactic acidosis if tissue perfusion is reduced due to severe volume loss and dehydration.


Acid-Base Balance: Traditional and Modified Approaches. Muir WW, deMorais H. Chapter 18 in Lumb and Jones' Veterinary Anesthesia, 3rd Edition. Thurmon JC, Tranquilli WJ, Benson GJ Eds. Williams & Wilkins, Baltimore. 1996.

Practical Approach to Acid-Base Disorders. Bailey JE, Pablo LS. in Veterinary Clinics of North America: Small Animal Practice. 28(3) pg. 645-62, May 1998.

Clinical Assessment of Acid-Base Status. Constable PD. In Veterinary Clinics of North America: Food Animal Practice. 15(3) pgs. 447-69, Nov 1999.

Fluid Therapy in Small Animal Practice DiBartola SP editor. WB Saunders, Philadelphia. 1992.

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