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Compendium October 2009 (Vol 31, No 10)

Beyond Blood Gases: Making Use of Additional Oxygenation Parameters and Plasma Electrolytes in the Emergency Room

by Ricardo Irizarry, Adam J. Reiss, DVM, DACVECC


    When provided with an emergency blood gas or electrolyte readout, clinicians must identify the critical parameters that require immediate intervention. This article provides concepts in oxygenation and electrolyte evaluation to help fine-tune the initial treatment and monitoring orders for emergency patients.

    Oxygenation Parameters

    Pao2/Fio2 Ratio

    Normal reference values for the alveolar–arterial (a–a) gradient can vary up to 100 mm Hg in animals receiving oxygen supplementation with a fraction of inspired oxygen (Fio2) >0.21.1 Therefore, when arterial blood gases for animals receiving oxygen supplementation are assessed, the ratio of the arterial partial pressure of oxygen (Pao2) to the Fio2 (Pao2/Fio2 or P/F ratio) allows objective estimation of oxygenation at different concentrations of inspired oxygen.2 A healthy small animal breathing room air (Fio2 = 0.21) should have a measured Pao2 approximating 100 mm Hg and a P/F ratio of around 500.2 Supplemented with 100% oxygen (Fio2 = 1.0), this same patient should have a measured Pao2 approximating 500 mm Hg and a similar P/F ratio. A P/F ratio >400 suggests that pulmonary function is normal. As respiratory function progressively decreases, the ratio decreases and approaches 200.3 In humans, a P/F ratio <200 meets the criteria for acute respiratory distress syndrome.4 In essence, the P/F ratio can help identify the adequacy of the patient's response to oxygen therapy. Pao2 is measured as part of the arterial blood gas analysis, whereas Fio2 can be measured with a handheld oximeter or estimated (TABLE 1).5,6

    Arterial Oxygen Saturation

    Pao2 serves as the driving force to push dissolved oxygen into hemoglobin molecules. Saturated hemoglobin is then responsible for carrying approximately 98% of the total blood oxygen content to tissue.7 The oxygen–hemoglobin dissociation curve depicts the relationship between Pao2 and arterial oxygen saturation (Sao2;FIGURE 1). A patient with a Pao2 of 60 mm Hg has an Sao2 of approximately 91%. This corresponds to a level of hypoxemia below which therapeutic intervention may be warranted.8 Further Pao2 reduction from 60 mm Hg causes stress to the patient, and even minor additional decreases in Pao2 are associated with significant oxygen dissociation from the hemoglobin molecules, as demonstrated by the steep portion of the curve.5

    Arterial Oxygen Content

    Sao2 provides no information about blood oxygen content because a patient can have a very low hemoglobin concentration (i.e., severe anemia) but still be fully saturated (Sao2 of 99% to 100%). The arterial oxygen content (Cao2) equation indicates how much oxygen is available to the tissues.7 It incorporates hemoglobin saturation (Sao2) and hemoglobin concentration ([Hb]) as well as the relatively minor contribution of unbound or freely dissolved oxygen (Pao2). The normal range of Cao2 is 16 to 20 mL oxygen/dL of blood.9 The following formula is used to calculate Cao25:

    [Hb] can be estimated by multiplying the measured hematocrit by one-third or can be measured with a hemoglobinometer10; the normal [Hb] is 15 mg/dL.8 The constant 1.34 is the amount of oxygen (in mL) that each gram of hemoglobin can bind when fully saturated. Sao2 is the actual percentage of oxygen saturation, and 0.003 is the solubility constant for dissolved (unbound) oxygen in plasma at body temperature.

    This calculation is useful in anemic patients, which can have Pao2 and Sao2 within normal limits while Cao2 remains markedly reduced until [Hb] is increased with a transfusion of blood or hemoglobin-based oxygen carrier.


    The anion gap (AGap) is an adjunct to blood gas evaluation that helps differentiate causes of metabolic acidosis. It is calculated as the difference between the measured plasma concentrations of the major positively charged ions (cations) and the major negatively charged ions (anions).11 In reality, the body always attempts to maintain electroneutrality, so the concentration of serum cations equals that of anions.12  FIGURE 2 shows the approximate plasma concentrations of cations and anions in healthy dogs and cats.13 The charge contributions of cations and anions must balance each other to maintain electrochemical neutrality.

    The AGap exists because standard electrolyte panels do not measure all the anions present in serum; thus, in general, the AGap represents the unmeasured anions (proteins, organic acids, and inorganic acids).3 In a healthy dog or cat, plasma proteins account for most of the AGap. As shown in FIGURE 3 , the AGap is calculated from four measured chemistry values: sodium (Na+), potassium (K+), chloride (Cl), and bicarbonate (HCO3) ion concentrations. The serum total carbon dioxide (TCO2) concentration can be used in place of the HCO3 concentration.14

    Metabolic acidosis, a very common acid–base disturbance in critically ill small animal patients, causes a reduction in HCO3 concentration.15 When there is an increase in unmeasured anions or in the Cl concentration, the HCO3 concentration decreases to maintain electrochemical balance.16 Thus, the AGap can be used to categorize metabolic acidosis as increased or hyperchloremic (normal AGap acidosis).17 Typical reference ranges are approximately 12 to 24 mEq/L in dogs and 13 to 27 mEq/L in cats.16

    Increased AGap acidosis arises when excess acid containing unmeasured anions (i.e., anions other than Cl) accumulates in the blood.16 Examples include lactic acidosis, ketoacidosis, uremic acidosis (phosphate and sulfate acidosis), ethylene glycol (antifreeze) poisoning, and salicylic acid (aspirin) poisoning.14 These excess anions titrate the HCO3 concentration downward, thus preserving electrochemical balance.12

    Metabolic acidosis characterized by a normal AGap arises when chloride, which is routinely measured, is added to the blood (e.g., dilutional acidosis with aggressive sodium chloride fluid administration)16 or when HCO3 loss from the body (e.g., associated with diarrhea18) is replaced with chloride to maintain electrochemical balance.15 Again, the excess Cl titrates the HCO3, thereby preserving the electrochemical balance.

    The first step in incorporating the AGap into the acid–base evaluation is to identify metabolic acidosis from the pH and the base excess of the extracellular fluid (or HCO3) value.a If metabolic acidosis is present, the adequacy of the normal physiologic compensatory reaction (i.e., decreased Pco2) should be determined. If the compensation is adequate, a simple acid–base disorder is present.3 The AGap should then be evaluated for the presence of high or normal AGap acidosis. If the AGap is normal, hyperchloremic metabolic acidosis is most likely present, although the AGap may be falsely normal in patients with low serum proteins (see Hypoalbuminemia section below). If the AGap is increased, high AGap acidosis is present and the bicarbonate gap should be calculated to help identify possible concurrent mixed metabolic disorders.

    The Bicarbonate Gap

    The bicarbonate gap is defined as the increase in the AGap from the midpoint of its reference range (ΔAGap) minus the change in HCO3 or serum TCO2 concentration from the midpoint of their respective reference ranges (ΔHCO3 or ΔTCO2;FIGURE 4).14

    It serves to identify nonparallel changes in HCO3 concurrent with high AGap acidosis.14 If AGap acidosis is the only acid–base abnormality, there should be a 1:1 correlation between the rise in AGap and the fall in HCO3,12 and the bicarbonate gap should be zero. For example, if the AGap goes up by 10 mEq/L, indicating high AGap metabolic acidosis, then the HCO3 or serum TCO2 should go down by 10 mEq/L. A bicarbonate gap other than zero suggests a mixed metabolic disorder.14,19 If the bicarbonate gap is positive, mixed AGap acidosis and concurrent metabolic alkalosis should be suspected. If the bicarbonate gap is negative, mixed AGap and hyperchloremic acidosis should be suspected.

    A positive bicarbonate gap suggests that the HCO3 value is higher than expected for a given concentration of unmeasured anions,12,14 which would develop, for example, in a vomiting patient with concurrent lactic acidosis from impaired tissue perfusion and hypochloremia from loss of hydrochloric acid in the vomitus. In this case, the AGap would be increased but the HCO3 level would not be equally decreased because of the concurrent Cl loss (FIGURE 5). This mixed metabolic disorder follows the laws of electroneutrality.

    In this patient, concurrent AGap acidosis and metabolic alkalosis may result in a blood pH that is close to normal. Analysis of the bicarbonate gap can therefore help reveal conditions that otherwise might not be immediately suspected (in this case, possible intestinal obstruction) and prompt therapy (administration of IV fluids) and further diagnostic tests (abdominal radiography).

    A negative bicarbonate gap suggests that the HCO3 value is lower than expected for a given concentration of unmeasured anions. This occurs with concurrent AGap and hyperchloremic acidosis.12,14 An example would be a patient treated for diabetic ketoacidosis. In this case, the AGap would be increased because of the keto acids, and the HCO3 level may be decreased in excess of the ketoacidosis because of concurrent Cl gain from aggressive use of acidifying crystalloids (FIGURE 6).

    The metabolic acidosis in this case could be severe because of the two concurrent sources of bicarbonate loss. The low blood pH may prompt the use of more alkalinizing IV fluid crystalloids.


    Because the AGap in healthy dogs and cats is mostly a result of the negative charge of serum proteins, hypoalbuminemia can lead to underestimation of high AGap metabolic acidosis.16,20 Patients with high levels of unmeasured anions (e.g., increased lactic acid due to hypotension) and concurrent hypoalbuminemia may have normal AGap measurements because the low albumin concentration causes the AGap to decrease, perhaps back to the reference range. In dogs, for each 1 g/dL decrease in albumin, there is a corresponding 4.1 mEq/L decrease in the AGap.18 The following formula can be used to correct the AGap for changes in albumin concentration and reveal an increased AGap acidosis18:

    Downloadable PDF

    1. Van Pelt DR, Wingfield WE, Wheeler SL, Salman MD. Oxygen-tension based indices as predictors of survival in critically ill dogs: clinical observations and review. J Vet Emerg Crit Care 1991;1(1):19-25.

    2. Clare M, Hopper K. Mechanical ventilation: indications, goals, and prognosis. Compend Contin Educ Pract Vet 2005;27(3):194-208.

    3. Bateman SW. Making sense of blood gas results. Vet Clin North Am Small Anim Pract 2008;38(3):543-557.

    4. Luce JM. Acute lung injury and the acute respiratory distress syndrome. Crit Care Med 1998;26(2):369-376.

    5. Camps-Palau MA, Marks SL, Cornick JL. Small animal oxygen therapy. Compend Contin Educ Pract Vet 1999;21(7):1-10.

    6. Tseng LW. Oxygen supplementation and humidification. In: Lesley KG, ed. Textbook of Respiratory Disease in Dogs and Cats. St Louis: WB Saunders; 2004:205-213.

    7. Martin L. PaO2, SaO2, and oxygen content. In: Martin L, ed. All You Really Need to Know to Interpret Arterial Blood Gases. 2nd ed. Baltimore: Lippincott Williams & Wilkins; 1999:75.

    8. Haskin S. Interpretation of blood gas measurements. In: Lesley KG, ed. Textbook of Respiratory Disease in Dogs and Cats. St Louis: WB Saunders; 2004:181-193.

    9. Davis H. Arterial and venous blood gases. In: Wingfield WE, Raffe MR, eds. The Veterinary ICU Book. Jackson, WY: Teton NewMedia; 2002:258-259.

    10. Mensack S, Murtaugh R. Oxygen toxicity. Compend Contin Educ Pract Vet 1999;21(4):341-350.

    11. Bailey JE, Pablo LS. Practical approach to acid-base disorders. Vet Clin North Am Small Anim Pract 1998;28(3):645-662.

    12. Martin L. pH, PaCO2, electrolytes, and acid-base status. In: Martin L, ed. All You Really Need to Know to Interpret Arterial Blood Gases. 2nd ed. Baltimore: Lippincott Williams & Wilkins; 1999:107-129.

    13. DiBartola SP. Introduction to acid-base disorders. In: Fluid, Electrolyte and Acid-Base Disorders in Small Animal Practice. 3rd ed. St. Louis: Elsevier; 2006:229-251.

    14. Adams LG, Polzin DJ. Mixed acid-base disorders. Vet Clin North Am Small Anim Pract 1989;

    15. Day TK. Blood gas analysis. Vet Clin North Am Small Anim Pract 2002;32(5):1031-1048.

    16. Kaae J, de Morais HA. Anion gap and strong ion gap: a quick reference. Vet Clin North Am Small Anim Pract 2008;38(3):443-447.

    17. Robertson SA. Simple acid-base disorders. Vet Clin North Am Small Anim Pract 1989;19(2):289-306.

    18. DiBartola SP. Mixed acid-base disorders. In: Fluid, Electrolyte and Acid-Base Disorders in Small Animal Practice. 3rd ed. St. Louis: Elsevier; 2006:296-309.

    19. Martin L. Primary and mixed acid base disorders. In: Martin L, ed. All You Really Need to Know to Interpret Arterial Blood Gases. 2nd ed. Baltimore: Lippincott Williams & Wilkins; 1999:136-137.

    20. Kellum JA. Clinical review: reunification of acid-base physiology. Crit Care 2005;9(5):500-507.

    Read the companion article, "Arterial and Venous Blood Gases: Indications, Interpretations, and Clinical Applications."

    aMore information about acid-base disturbances is available in the companion article, "Arterial and Venous Blood Gases: Indications, Interpretations, and Clinical Applications."

    References »

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