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Compendium October 2009 (Vol 31, No 10)

Arterial and Venous Blood Gases: Indications, Interpretations, and Clinical Applications

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

    CETEST This course is approved for 3.0 CE credits

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    Blood gas analysis is frequently requested as part of the point-of-care testing for emergency or critical care patients presenting with metabolic or respiratory abnormalities. With the advent of portable units, information regarding a patient's acid-base, ventilation, and oxygenation status can be rapidly obtained. This article provides essential information on arterial and venous blood gas analysis with the goal of helping clinicians integrate such data in their case management.

    Metabolic derangements and respiratory distress are common presenting problems in emergency medicine.1 A focused physical examination and emergency intervention should precede any diagnostic testing if the clinical condition of the patient dictates such urgent care. After the patient is stabilized, a history should be taken and the patient's hydration, ventilation, and oxygenation status assessed. The patient's electrolyte levels and acid-base status (pH) should also be determined.


    Blood gas analysis can help assess underlying disease processes and the severity of illness and can guide emergency interventions (e.g., IV fluid administration, oxygen therapy, electrolyte supplementation, positive-pressure ventilation).2

    Arterial blood gases primarily provide information regarding oxygenation (i.e., oxygen loading from the lungs into the blood), ventilation (i.e., carbon dioxide (CO2) off-loading from the blood into the lungs), and acid-base status. Venous blood gases can provide information on acid-base status and ventilation (i.e., venous partial pressure of CO2 (Pvco2)).3,4 In adequately perfused patients, the Pvco2 is normally 4 to 6 mm Hg higher than the arterial partial pressure of CO2 (Paco2); the difference can be greater in severely hypoperfused patients.5

    Arterial samples are particularly useful in assessing the patient's oxygenation and ventilation status. For example, the oxygenation status can be evaluated by measuring the arterial partial pressure of oxygen (Pao2) and using this value in additional calculations, as described in step 5 below.6,a Arterial samples are usually collected from the dorsal pedal artery, femoral artery, or, in anesthetized patients, sublingual artery. Step-by-step instructions for sample collection techniques can be found elsewhere.7,8


    Point-of-care blood gas analyzers directly measure the pH, partial pressure of oxygen (Po2), and partial pressure of CO2 (Pco2). These measured values are then used to derive the percentage of hemoglobin saturated with oxygen (SO2), bicarbonate (HCO3-) concentration, total CO2 (TCO2) concentration, and base excess of the extracellular fluid (BEecf). The SO2 is usually determined by the Po2 from the oxygen dissociation curve. The HCO3- concentration, TCO2 concentration, and BEecf are also derived from formulas and nomograms.  BOX 1 lists some of the analytes typically reported by point-of-care analyzers.

    The BEecf, HCO3- concentration, and TCO2 concentration all serve as measures of the metabolic component of the patient's acid-base status, whereas Pco2 evaluates ventilation and represents the respiratory component of the acid-base status.9 Oxygenation, as calculated from the Pao2, is also part of the respiratory component.

    Step-By-Step Approach to Arterial and Venous Blood Gas Analysis

    Step 1: pH

    The blood pH represents the overall balance of all the acid (acidotic) and base (alkalotic) processes in the body.7,10 It is determined by the ratio between the metabolic (HCO3-) and respiratory (Pco2) components of the acid-base balance.11

    In general, acidemia is defined as a blood pH below 7.35 and alkalemia as a blood pH above 7.45 (7.4 is neutral).10 Based on the Henderson-Hasselbalch equation, the pH can be defined by the ratio of the HCO3- concentration ([HCO3-]) to the dissolved CO2 concentration ([αPco2]) in the extracellular fluid12:

    In this equation, α is the solubility coefficient for CO2, and it equals 0.03.

    A good rule is that pH generally changes in the same direction as the primary disorder.12

    Step 2: Evaluate the Respiratory Component

    Pco2 provides information regarding ventilation, or the respiratory component of acid"base balance.13 Alveolar ventilation is defined as the volume of gas per unit time that reaches the alveoli, where gas exchange with pulmonary blood occurs.14

    Hypoventilation is characterized by increases in Pco2 (>45 mm Hg) as CO2 is retained in the blood. CO2 is a volatile acid, so retention of CO2 leads to respiratory acidosis.15 In most instances, respiratory acidosis is caused by some aspect of ventilatory failure, whereby normal amounts of CO2 produced by tissue metabolism cannot be properly excreted by alveolar minute ventilation.13 Common causes of hypoventilation include those affecting neurologic control of respiration (e.g., anesthesia, sedation), breathing mechanics (e.g., diaphragmatic hernia, pleural space disease), or proper flow of air through the airways (e.g., upper or lower airway obstruction) or the alveoli.15

    Hyperventilation is characterized by decreases in Pco2 as the CO2 is blown off from the alveoli, which leads to respiratory alkalosis (Pco2 <35 mm Hg).16 Causes of hyperventilation include hypoxemia, pulmonary disease, pain, anxiety, and overzealous manual or mechanical ventilation. Hyperventilation may also develop as a compensation for metabolic acidosis.16

    Although oxygenation may not directly affect the acid-base balance, it should be assessed in critically ill patients.

    Step 3: Evaluate the Metabolic Component

    The metabolic contribution to the acid-base balance can be assessed with the HCO3- concentration and the BEecf.12,17 Typical reference ranges for HCO3- are 19 to 23 mEq/L in dogs and 17 to 21 mEq/L in cats.18 Values less than these ranges indicate metabolic acidosis, whereas values greater than the ranges indicate metabolic alkalosis.

    As mentioned above, the HCO3- concentration is calculated from the pH and Pco2; thus, it is not independent of respiratory activity.19 In an attempt to isolate the metabolic component from respiratory influences, the concept of BEecf was developed.17 The BEecf takes into account all of the body's buffer systems, including HCO3-, to predict the quantity of acid or alkali required to return the extracellular fluid compartment to neutrality (pH = 7.4) while the Paco2 is held constant at 40 mm Hg.10 By standardizing for the effects of the respiratory component, the BEecf is representative of all the metabolic acid-base disturbances in a patient.17 Normally, the BEecf is 0 ± 4 mEq/L.12 Lower values (BEecf <-4) indicate metabolic acidosis, whereas higher values (BEecf >+4) indicate metabolic alkalosis.

    Metabolic acidosis can be caused by increases in the generation of hydrogen ions (H+) from endogenous (e.g., lactate, ketones) or exogenous acids (e.g., ethylene glycol, salicylates) and by the inability of the kidneys to excrete H+ from dietary protein (renal failure). These increases in H+ in the body are buffered by decreases in HCO3-, producing a lowered HCO3-:Pco2 ratio and, subsequently, a lowered pH. In addition, metabolic acidosis can be caused by a direct loss of bicarbonate (HCO3-) through the gastrointestinal tract (diarrhea) or kidneys (renal tubular acidosis) or, less commonly, by the aggressive use of intravenous fluids that contain no bicarbonate or bicarbonate precursors (e.g., saline).12 Metabolic alkalosis can occur from a loss of H+ (vomiting of stomach contents) or from a gain of HCO3- (e.g., sodium bicarbonate administration, hypochloremic alkalosis caused by the use of loop diuretics).20

    Step 4: Evaluate the Compensatory Response

    Simple acid-base disorders are caused by the four primary acid-base disturbances, metabolic or respiratory in origin, with an anticipated compensatory change9 (TABLE 1). The primary disorder leads to a change in pH, while compensatory changes attempt to normalize the HCO3-:Pco2 ratio and bring the pH back to neutral. Compensatory changes in Pco2 and HCO3- parallel each other, as shown by the direction of the arrows in each row in TABLE 1 .

    Typically, pH changes arising from one component (e.g., metabolic) are opposed by changes in the other component (e.g., respiratory) to maintain the proper ratio of metabolic to respiratory contribution to the overall pH.10,21 For example, with metabolic acidosis, the HCO3- concentration decreases, thereby lowering the HCO3-:Pco2 ratio and resulting in acidemia (pH <7.35).12 In most instances, the body compensates by decreasing the Pco2 or hyperventilating in an attempt to maintain the ratio (i.e., ↓HCO3-:↓Pco2). In other words, the respiratory component compensates for the metabolic acidosis in an attempt to raise the pH to neutral. Physiologic compensation rarely completely resolves the primary acid-base abnormality and never leads to overcompensation. Therefore, the pH typically deviates from neutral even after adequate compensation, although it can be within the reference range in patients with mild acid-base disorders.22

    For example, in TABLE 2 , the patient is in acute respiratory failure, with primary respiratory acidosis (Paco2 = 65 mm Hg), severe hypoxemia (Pao2 = 45 mm Hg), and HCO3- accumulation (HCO3- = 26 mEq/L). The pH indicates acidemia, and the Paco2 indicates hypercapnia; therefore, the system responsible for the acidemia in this patient is the respiratory system. In this case, hypoventilation (represented by increased Paco2) decreases the HCO3-:Pco2 ratio, thus lowering the pH. Given the mild increase in HCO3-, there appears to be a mild metabolic compensation, but this increase is more likely attributable to respiratory influences on the HCO3- concentration. The BEecf suggests a trend toward metabolic compensation that has not yet been truly achieved. However, if this condition persists for longer than 48 hours, the kidneys will have enough time to retain HCO3- in an attempt to compensate for what would then be considered chronic respiratory acidosis, resulting in notable increases in the HCO3- and BEecf values (e.g., 38 mEq/L and +10 mEq/L, respectively).13 Again, note that physiologic compensation for a primary acid-base disturbance is almost never able to return pH to neutral.

    Metabolic acidosis is the most common acid-base disturbance in small animals.1 If metabolic acidosis is the primary disturbance, it will be represented by a lower pH, a negative BEecf or lower HCO3- concentration, and a compensatory decrease in the Pco2 in an attempt to blow off excess acid load. The adequacy of the compensatory response can be quantified with the use of formulas that predict the expected response to the primary disturbance (TABLE 3).21 These responses have not been objectively evaluated in cats, but in most cases, cats' responses are assumed to be similar to those of dogs.17 Acute responses last less than 2 days, whereas chronic responses may take 2 to 5 days to reach maximal effect.

    By quantifying the degree of compensatory changes and comparing with the expected (calculated) values, clinicians can assess whether the patient's values are within or outside a defined margin of error. If they are within the margin, the patient has a primary disturbance and is compensating adequately; if they are outside it, the patient likely has multiple primary acid-base disorders (a mixed acid-base disorder).17 For example, inappropriate respiratory compensation (Pco2) for metabolic acidosis (↓HCO3-) is diagnosed by comparing the measured Pco2 with the expected (i.e., calculated) changes in Pco2 predicted for each mEq/L decrease in HCO3- (first row in TABLE 3). When the measured Pco2 is lower than expected, primary respiratory alkalosis is complicating the metabolic acidosis. An example of a patient with such a mixed disturbance would be a hyperventilating dog with renal failure. Pain, fear, and excitement can cause hyperventilation (decreased Pco2) in excess of the calculated compensation for metabolic acidosis, which, in this patient, is a result of the uremic acidosis associated with renal failure. Conversely, when the measured Pco2 is higher than expected, primary respiratory acidosis is complicating the metabolic acidosis. An example would be a trauma patient (e.g., hit by a car) with lactic acidosis from shock and hypoventilation (increased Pco2) from pneumothorax preventing proper lung expansion.

    In summary, a simple acid-base disturbance should be suspected when the patient meets expected compensation values, and a mixed disturbance should be suspected when compensation does not fall within the expected values.23 In addition, a mixed disturbance should be suspected when the pH is within the reference range but Pco2 and HCO3- values are not or when Pco2 and HCO3- concentrations change in opposite, not parallel, directions.6

    Step 5: Evaluate Oxygenation

    Hypoxemia refers to a reduction of oxygen in the arterial blood, indicated by Pao2 values below 80 mm Hg.6 The presence of hypoxemia can be life-threatening, and a Pao2 value below 60 mm Hg warrants immediate therapeutic intervention.4 Any time a low Pao2 is obtained from a patient breathing room air, the alveolar gas equation should be used to determine the alveolar-arterial (a-a) oxygen gradient (see below).6 Normal values for the a-a gradient are 5 to 15 mm Hg. By accounting for the effects of altitude, fraction of inspired oxygen (Fio2), and ventilation on the patient's oxygenation, the a-a oxygen gradient provides a measure of the adequacy of oxygen transfer across the alveolar membrane into the pulmonary capillaries perfusing the alveoli (i.e., oxygen loading into the blood).24,25 Serial calculations of the a-a oxygen gradient allow for objective estimates of pulmonary function over time.24,26

    Most pulmonary diseases alter the ventilation:perfusion ratio (i.e., V./Q. mismatch) of individual alveoli, which leads to a reduction in oxygen loading into the blood and a corresponding lower Pao2 (FIGURE 1 and BOX 2).26 V./Q. mismatches lead to an increase in the a-a gradient. The calculations used to quantify pulmonary gas exchange efficacy in the presence of hypoxemia (Pao2 <80 mm Hg) at room air and obtain the a-a gradient are as follows4,24:

    Alveolar gas equation: Alveolar partial pressure of oxygen (Pao2) = [Fio2 × (PB - 47)] - (1.2 × Paco2)

    In these equations, PB is atmospheric pressure (760 mm Hg at sea level), and 47 is the water vapor pressure in mm Hg (which is subtracted because only dry alveolar gas pressures are measured). The factor 1.2 represents the respiratory quotient, or the ratio of oxygen uptake to CO2 exhaled.  FIGURE 1 helps illustrate the concept.

    The following equation is a simplified version of the alveolar gas equation that can be used for patients breathing room air (Fio2 = 0.21) at sea level (PB = 760 mm Hg)24:

    Clinically, a normal a-a gradient (5 to 15 mm Hg) excludes pulmonary disease and suggests that arterial hypoxemia (Pao2 <80 mm Hg) is due to hypoventilation (increased Paco2) or decreased inspired oxygen.26 Patients with a gradient above 25 mm Hg should be considered to have a degree of V./Q. mismatch from pulmonary parenchymal disease, although cardiovascular pathology can also affect this value.17,26


    Blood gas analysis helps assess three vital physiologic processes in critically ill veterinary patients: acid-base status, ventilation, and oxygenation. Initial blood gas analysis helps diagnose underlying disease processes and guide therapeutic interventions. Serial measurements can be used to assess proper response to therapy. Blood gas analysis requires a step-by-step approach and practice. Blood gas data should always be interpreted in light of full clinical and laboratory information.

    Downloadable PDF

    1. Cornelius LM, Rawlings CA. Arterial blood gas and acid-base values in dogs with various diseases and signs of disease. JAVMA 1981;178(9):992-995.

    2. Mathews K. Acid-base assessment. In: Mathews K, ed. Veterinary Emergency and Critical Care Manual. 2nd ed. Guelph, ON: LifeLearn; 2006:406-410.

    3. Ilkiw JE, Rose RJ, Martin IC. A comparison of simultaneously collected arterial, mixed venous, jugular venous and cephalic venous blood samples in the assessment of blood-gas and acid-base status in the dog. J Vet Intern Med 1991;5(5):294-298.

    4. 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.

    5. Wingfield WE, Van Pelt DR, Hackett TB, et al. Usefulness of venous blood in estimating acid-base status of the seriously ill dog. J Vet Emerg Crit Care 1994;4(1):23-27.

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

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

    8. Ford RB, Mazzaferro EM. Diagnostics and therapeutic procedures: advanced procedures. In: Winkel AJ, ed. Kirk and Bistner's Handbook of Veterinary Procedures and Emergency Treatment. 8th ed. St. Louis: Saunders Elsevier; 2006:508-509.

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

    10. Haskins SC. An overview of acid-base physiology. JAVMA 1977;170(4):423-428.

    11. McNamara J, Worthley LI. Acid-base balance: part I. Physiology. Crit Care Resusc 2001;3(3):181-187.

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

    13. Wall RE. Respiratory acid-base disorders. Vet Clin North Am Small Anim Pract 2001;31(6):1355-1367.

    14. Guyton AC, Hall JE. Pulmonary ventilation. In: Textbook of Medical Physiology. 11th ed. Philadelphia: Elsevier Saunders; 2006:477.

    15. Johnson RA. Respiratory acidosis: a quick reference. Vet Clin North Am Small Anim Pract 2008;

    16. Johnson RA. Respiratory alkalosis: a quick reference. Vet Clin North Am Small Anim Pract 2008;38(3):427-430.

    17. Bateman SW. Making sense of blood gas results. Vet Clin North Am Small Anim Pract 2008;

    18. de Morais HA. Metabolic acidosis: a quick reference. Vet Clin North Am Small Anim Pract 2008;

    19. Constable PD. Clinical assessment of acid-base status: comparison of the Henderson-Hasselbalch and strong ion approaches. Vet Clin Pathol 2000;29(4):115-128.

    20. Foy D, de Morais HA. Metabolic alkalosis: a quick reference. Vet Clin North Am Small Anim Pract 2008;38(3):435-438.

    21. Autran de Morais HS, Dibartola SP. Ventilatory and metabolic compensation in dogs with acid-base disturbances. J Vet Emerg Crit Care 1991;1(2):39-49.

    22. 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.

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

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

    25. 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.

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

    aMore information about calculating additional oxygenation parameters is available in the companion article, "Beyond Blood Gases: Making Use of Additional Oxygenation Parameters and Plasma Electrolytes in the Emergency Room."

    References »

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

    CETEST This course is approved for 3.0 CE credits

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