3 CE CREDITS CE Article

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

❯❯ Ricardo Irizarry, DVM Abstract: Blood gas analysis is frequently requested as part of the point-of-care testing for emer- Adam Reiss, DVM, gency or critical care patients presenting with metabolic or respiratory abnormalities. With the ad- DACVECC vent of portable units, information regarding a patient’s acid–base, ventilation, and oxygenation sta- Southern Oregon Veterinary Specialty Center tus can be rapidly obtained. This article provides essential information on arterial and venous blood Medford, Oregon gas analysis with the goal of helping clinicians integrate such data in their case management.

etabolic derangements and respi- the difference can be greater in severely ratory distress are common pre- hypoperfused patients.5 senting problems in emergency Arterial samples are particularly use- M 1 medicine. A focused physical examina- ful in assessing the patient’s oxygenation tion and emergency intervention should and ventilation status. For example, the precede any diagnostic testing if the clini- oxygenation status can be evaluated by At a Glance cal condition of the patient dictates such measuring the arterial partial pressure

Indications urgent care. After the patient is stabilized, of oxygen (Pao2) and using this value in Page E1 a history should be taken and the patient’s additional calculations, as described in Analytes hydration, ventilation, and oxygenation step 5 below.6,a Arterial samples are usu- Page E1 status assessed. The patient’s electrolyte ally collected from the dorsal pedal , Step-By-Step levels and acid–base status (pH) should femoral artery, or, in anesthetized patients, Approach to Arterial also be determined. sublingual artery. Step-by-step instructions and Venous Blood for sample collection techniques can be 7,8 Gas Analysis Indications found elsewhere. Page E2 Blood gas analysis can help assess under- The Four Primary Acid– lying disease processes and the severity of Analytes Base Disorders and Their illness and can guide emergency interven- Point-of-care blood gas analyzers directly Compensatory Changes tions (e.g., IV fluid administration, oxygen measure the pH, partial pressure of oxy- Page E3 therapy, electrolyte supplementation, pos- gen (Po2), and partial pressure of CO2 itive-pressure ventilation).2 (Pc o ). These measured values are then Sample Gas 2 Arterial blood gases primarily pro- used to derive the percentage of hemo- Report From a Patient With vide information regarding oxygenation globin saturated with oxygen (SO2), bicar- Acute Respiratory Failure – Page E3 (i.e., oxygen loading from the into bonate (HCO3 ) concentration, total CO2

the blood), ventilation (i.e., carbon diox- (TCO2) concentration, and base excess of Summary of Compensatory ide (CO ) off-loading from the blood into the extracellular fluid (BEecf). The SO is Responses in Dogs With 2 2 the lungs), and acid–base status. Venous usually determined by the Po from the Metabolic and Respiratory 2 blood gases can provide information oxygen dissociation curve. The HCO – Acid–Base Disorders 3 Page E3 on acid–base status and ventilation (i.e., 3,4 aMore information about calculating additional venous partial pressure of CO2 (Pvc o 2)). oxygenation parameters is available in the com- In adequately perfused patients, the Pvc o 2 panion article, “Beyond Blood Gases: Making is normally 4 to 6 mm Hg higher than the Use of Additional Oxygenation Parameters and

arterial partial pressure of CO2 (Pac o 2); Plasma Electrolytes in the Emergency Room.”

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FREE CE Blood Gases: Interpretations and Clinical Applications

Box 1 A good rule is that pH generally changes in Typical Analytes the same direction as the primary disorder.12 Provided by Point-of-Care Step 2: Evaluate the Respiratory Blood Gas Analyzers Component

Pc o 2 provides information regarding ventila- Venous Arterial tion, or the respiratory component of acid– ❯ pH ❯ pH base balance.13 Alveolar ventilation is defined

❯ Pc o 2 ❯ Pc o 2 as the volume of gas per unit time that reaches a ❯ TCO2 ❯ Po2 the alveoli, where gas exchange with pulmo- –a a 14 ❯ HCO3 ❯ TCO2 nary blood occurs. a –a ❯ BEecf ❯ HCO3 Hypoventilation is characterized by increases a ❯ BEecf in Pc o 2 (>45 mm Hg) as CO2 is retained in a ❯ SO2 the blood. CO2 is a volatile acid, so retention 15 aCalculated value. of CO2 leads to respiratory acidosis. In most instances, respiratory acidosis is caused by some aspect of ventilatory failure, whereby

concentration, TCO2 concentration, and BEecf normal amounts of CO2 produced by tissue are also derived from formulas and nomo- metabolism cannot be properly excreted by QuickNotes grams. Box 1 lists some of the analytes typi- alveolar minute ventilation.13 Common causes The most common cally reported by point-of-care analyzers. of hypoventilation include those affecting neu- – acid–base distur- The BEecf, HCO3 concentration, and TCO2 rologic control of respiration (e.g., anesthesia, bance encountered concentration all serve as measures of the sedation), breathing mechanics (e.g., diaphrag- in small animals metabolic component of the patient’s acid– matic hernia, pleural space disease), or proper base status, whereas Pc o 2 evaluates ventilation flow of air through the airways (e.g., upper or is metabolic and represents the respiratory component of lower airway obstruction) or the alveoli.15 acidosis, which the acid–base status.9 Oxygenation, as calcu- Hyperventilation is characterized by de­-

is represented lated from the Pao2, is also part of the respira- creases in Pc o 2 as the CO2 is blown off from by a lower pH, a tory component. the alveoli, which leads to respiratory alkalosis 16 negative BEecf or (Pc o 2 <35 mm Hg). Causes of hyperventilation – Step-By-Step Approach to Arterial and include hypoxemia, pulmonary disease, pain, lower HCO3 concentration, and Venous Blood Gas Analysis anxiety, and overzealous manual or mechanical a compensatory Step 1: pH ventilation. Hyperventilation may also develop The blood pH represents the overall balance as a compensation for metabolic acidosis.16 decrease in the of all the acid (acidotic) and base (alkalotic) Although oxygenation may not directly Pc o 2 in an attempt processes in the body.7,10 It is determined by affect the acid–base balance, it should be – to blow off excess the ratio between the metabolic (HCO3 ) and assessed in critically ill patients.

acid load. respiratory (Pc o 2) components of the acid– base balance.11 Step 3: Evaluate the Metabolic In general, acidemia is defined as a blood Component pH below 7.35 and alkalemia as a blood pH The metabolic contribution to the acid–base 10 – above 7.45 (7.4 is neutral). Based on the balance can be assessed with the HCO3 con- Henderson–Hasselbalch equation, the pH centration and the BEecf.12,17 Typical refer- – – can be defined by the ratio of the HCO3 ence ranges for HCO3 are 19 to 23 mEq/L in – 18 concentration ([HCO3 ]) to the dissolved CO2 dogs and 17 to 21 mEq/L in cats. Values less

concentration ([αPc o 2]) in the extracellular than these ranges indicate metabolic acidosis, fluid12: whereas values greater than the ranges indi- cate metabolic alkalosis. – [HCO3 ] (metabolic) – pH ≈ As mentioned above, the HCO3 concentra- c o [αP 2] (respiratory) tion is calculated from the pH and Pc o 2; thus, it is not independent of respiratory activity.19 In this equation, α is the solubility coefficient In an attempt to isolate the metabolic compo-

for CO2, and it equals 0.03. nent from respiratory influences, the concept

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FREE Blood Gases: Interpretations and Clinical Applications CE of BEecf was developed.17 The BEecf takes table 1 The Four Primary Acid–Base Disorders and into account all of the body’s buffer systems, a – Their Compensatory Changes including HCO3 , to predict the quantity of acid or alkali required to return the extracellu- Conditions Primary Disorder Compensation lar fluid compartment to neutrality (pH = 7.4) – ↓pH and ↓HCO3 (↓BEecf) Metabolic acidosis ↓Pc o 2 10 while the Pac o 2 is held constant at 40 mm Hg. By standardizing for the effects of the respira- – ↑pH and ↑HCO3 (↑BEecf) Metabolic alkalosis ↑Pc o 2 tory component, the BEecf is representative of – all the metabolic acid–base disturbances in a ↓pH and ↑Pc o 2 Respiratory acidosis ↑HCO3 (↑BEecf) patient.17 Normally, the BEecf is 0 ± 4 mEq/L.12 – Lower values (BEecf <–4) indicate metabolic ↑pH and ↓Pc o 2 Respiratory alkalosis ↓HCO3 (↓BEecf) acidosis, whereas higher values (BEecf >+4) aRose BD, Post TW. Introduction to simple and mixed acid–base disorders. In: Clinical Physiology of Acid–Base and Electrolyte 5th ed. New York: McGraw-Hill Book Co; 2001:541. indicate metabolic alkalosis. Disorders. Metabolic acidosis can be caused by increases in the generation of hydrogen ions (H+) from endogenous (e.g., lactate, ketones) or exogenous table 2 Sample Arterial Blood Gas Report From a acids (e.g., ethylene glycol, salicylates) and by the inability of the kidneys to excrete H+ from dietary Patient With Acute Respiratory Failure protein (renal failure). These increases in H+ in the Analyte Value Reference Range – body are buffered by decreases in HCO3 , produc- – pH 7.22 7.35–7.45 ing a lowered HCO3 :Pc o 2 ratio and, subsequently, a lowered pH. In addition, metabolic acidosis can Pac o 2 65 mm Hg 36–40 mm Hg – be caused by a direct loss of bicarbonate (HCO3 ) through the gastrointestinal tract (diarrhea) or kid- Pao2 45 mm Hg 90–100 mm Hg neys (renal tubular acidosis) or, less commonly, by – the aggressive use of intravenous fluids that con- HCO3 26 mEq/L 20–24 mEq/L tain no bicarbonate or bicarbonate precursors (e.g., saline).12 Metabolic alkalosis can occur from a loss BEecf +4 mEq/L –4 to +4 mEq/L of H+ (vomiting of stomach contents) or from a – gain of HCO3 (e.g., sodium bicarbonate adminis- tration, hypochloremic alkalosis caused by the use of loop diuretics).20 table 3 Summary of Compensatory Responses in Dogs Step 4: Evaluate the Compensatory With Metabolic and Respiratory Acid–Base Disorders21 Response Primary Disorder Expected Compensation Simple acid–base disorders are caused by the four primary acid–base disturbances, metabolic Metabolic acidosis: ↓Pc o 2 of 0.7 mm Hg per 1.0 mEq/L decrease in HCO – ( BEecf) [HCO –] (±3) or respiratory in origin, with an anticipated ↓ 3 ↓ 3 compensatory change9 (Table 1). The primary Metabolic alkalosis: ↑Pc o 2 of 0.7 mm Hg per 1.0 mEq/L increase in disorder leads to a change in pH, while com- – – ↑HCO3 (↑BEecf) [HCO3 ] (±3) pensatory changes attempt to normalize the – HCO3 :Pc o 2 ratio and bring the pH back to neu- – Acute respiratory acidosis: ↑[HCO3 ] of 0.15 mEq/L per 1.0 mm Hg increase in c o – tral. Compensatory changes in P 2 and HCO3 ↑Pc o 2 Pc o 2 (±2) parallel each other, as shown by the direction – of the arrows in each row in Table 1. Chronic respiratory acidosis: ↑[HCO3 ] of 0.35 mEq/L per 1.0 mm Hg increase in Typically, pH changes arising from one com- ↑Pc o 2 Pc o 2 (±2) ponent (e.g., metabolic) are opposed by changes – in the other component (e.g., respiratory) to main- Acute respiratory alkalosis: ↓[HCO3 ] of 0.25 mEq/L per 1.0 mm Hg decrease in ↓Pc o Pc o (±2) tain the proper ratio of metabolic to respiratory 2 2 contribution to the overall pH.10,21 For example, Chronic respiratory alkalosis: [HCO –] of 0.55 mEq/L per 1.0 mm Hg decrease in – ↓ 3 with metabolic acidosis, the HCO3 concentration ↓Pc o 2 Pc o 2 (±2) – decreases, thereby lowering the HCO3 :Pc o 2 ratio [HCO –] = bicarbonate concentration and resulting in acidemia (pH <7.35).12 In most 3

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FREE CE Blood Gases: Interpretations and Clinical Applications

FIGURE 1 O2 bolic compensation, but this increase is more

O2 Pa o 2 ≈ 105 mm Hg likely attributable to respiratory influences on – O2 Pa c o 2 ≈ 37 mm Hg the HCO3 concentration. The BEecf suggests a O O2 2 trend toward metabolic compensation that has O O2 2 O not yet been truly achieved. However, if this O 2 O O 2 CO 2 2 2 O condition persists for longer than 48 hours, the O O 2 2 O 2 – 2 kidneys will have enough time to retain HCO3 CO CO2 2 O2 Pao ≈ 100 mm Hg in an attempt to compensate for what would O2 O2 2 Pac o 2 ≈ 37 mm Hg then be considered chronic respiratory acidosis, O – O 2 O2 O CO 2 O 2 O resulting in notable increases in the HCO3 and O 2 O 2 O 2 2 2 2 CO2 CO2 BEecf values (e.g., 38 mEq/L and +10 mEq/L, O2 O O2 O O O2 O 2 2 2 13 O2 O 2 O CO O 2 2 2 O 2 respectively). Again, note that physiologic com- CO 2 O2 CO2 O 2 CO 2 O O 2 pensation for a primary acid–base disturbance 2 2 O2 CO2 O2 O2 O is almost never able to return pH to neutral. O O O2 O 2 2 2 2 Metabolic acidosis is the most common O2 (IN) (OUT) O 2 1 Mixed venous blood Venous admixture Arterial blood acid–base disturbance in small animals. If metabolic acidosis is the primary disturbance, Cross-section of the alveoli–pulmonary circulation interface showing it will be represented by a lower pH, a nega-

oxygen (O2) and carbon dioxide (CO2) pressures. The depicted Pa o 2 is – tive BEecf or lower HCO3 concentration, and obtained from the alveolar gas equation by using normal reference values (e.g., a compensatory decrease in the Pc o 2 in an Pa o = 150 – [1.2 × 38 mm Hg] ≈ 105 mm Hg). The Pao is slightly lower than the 2 2 attempt to blow off excess acid load. The Pa o 2 because of physiologic venous admixture (Box 2). With pulmonary disease, the degree of admixture may increase, thus increasing the oxygen pressure gradi- adequacy of the compensatory response can ent between the alveoli and the systemic arterial circulation (i.e., the alveolar– be quantified with the use of formulas that arterial gradient). (Modified with permission from Martin L, ed. All You Really Need predict the expected response to the primary to Know to Interpret Arterial Blood Gases. 2nd ed. Baltimore: Lippincott Williams & disturbance (Table 3).21 These responses have Wilkins; 1999:70.) Pa c o 2 = alveolar partial pressures of CO2; Pac o 2 = arterial partial not been objectively evaluated in cats, but in pressures of CO ; Pa o = alveolar partial pressures of oxygen; Pa o = arterial par- 2 2 2 most cases, cats’ responses are assumed to be tial pressures of oxygen. similar to those of dogs.17 Acute responses last less than 2 days, whereas chronic responses instances, the body compensates by decreas- may take 2 to 5 days to reach maximal effect.

ing the Pc o 2 or hyperventilating in an attempt to By quantifying the degree of compensatory – maintain the ratio (i.e., ↓HCO3 :↓Pc o 2). In other changes and comparing with the expected (cal- words, the respiratory component compensates culated) values, clinicians can assess whether the QuickNotes for the metabolic acidosis in an attempt to raise patient’s values are within or outside a defined the pH to neutral. Physiologic compensation margin of error. If they are within the margin, the Oxygenation can rarely completely resolves the primary acid–base patient has a primary disturbance and is compen- be assessed by abnormality and never leads to overcompensa- sating adequately; if they are outside it, the patient tion. Therefore, the pH typically deviates from likely has multiple primary acid–base disorders Pao2 measurements obtained from an neutral even after adequate compensation, (a mixed acid–base disorder).17 For example, in­- although it can be within the reference range in appropriate respiratory compensation (Pc o 2) for arterial sample. 22 – patients with mild acid–base disorders. metabolic acidosis (↓HCO3 ) is diagnosed by

For example, in Table 2, the patient is in comparing the measured Pc o 2 with the expected

acute respiratory failure, with primary respi- (i.e., calculated) changes in Pc o 2 predicted for – ratory acidosis (Pac o 2 = 65 mm Hg), severe each mEq/L decrease in HCO3 (first row in – hypoxemia (Pao2 = 45 mm Hg), and HCO3 accu- Table 3). When the measured Pc o 2 is lower than – mulation (HCO3 = 26 mEq/L). The pH indicates expected, primary respiratory alkalosis is com-

acidemia, and the Pac o 2 indicates hypercapnia; plicating the metabolic acidosis. An example of therefore, the system responsible for the aci- a patient with such a mixed disturbance would demia in this patient is the respiratory system. be a hyperventilating dog with renal failure. Pain, In this case, hypoventilation (represented by fear, and excitement can cause hyperventilation – increased Pac o 2) decreases the HCO3 :Pc o 2 ratio, (decreased Pc o 2) in excess of the calculated com- thus lowering the pH. Given the mild increase pensation for metabolic acidosis, which, in this – in HCO3 , there appears to be a mild meta- patient, is a result of the uremic acidosis asso-

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ciated with renal failure. Conversely, when the Box 2 measured Pc o is higher than expected, primary 2 Ventilation:Perfusion Ratios: respiratory acidosis is complicating the metabolic acidosis. An example would be a trauma patient Shunts and Venous Admixture (e.g., hit by a car) with lactic acidosis from shock Venous admixture occurs when blood passes through the pulmonary cap- and hypoventilation (increased Pc o 2) from pneu- mothorax preventing proper expansion. illaries without being properly oxygenated by the alveoli (Figure 1). De- In summary, a simple acid–base disturbance pending on the severity. of. the admixture, it can be considered. a .shunt (i.e.,. . should be suspected when the patient meets ventilation:perfusion [V/Q] ratio. .= 0) or cause a decreased V/Q ratio (V/Q a 26 expected compensation values, and a mixed dis- ratio <1 but not 0). The ideal V/Q ratio is 1. turbance should be suspected when compensa- A shunt occurs when zero to very minimal ventilation occurs in alveoli that are still adequately perfused by pulmonary capillaries. Shunts can be physi- tion does not fall within the expected values.23 ologic or anatomic.a In the former, there is a severe physiologic redistribution In addition, a mixed disturbance should be of pulmonary blood flow away from collapsed or markedly infiltrated alveoli (as suspected when the pH is within the reference seen with lobar atelectasis and with severe pneumonia, pulmonary contusions, range but Pc o and HCO – values are not or when 2 3 or pulmonary edema). In the latter, there is an anatomic diversion of blood Pc o and HCO – concentrations change in oppo- 2 3 away from the pulmonary circulation (as seen with right to left shunting from a 6 site, not parallel, directions. ventricular septal defect or a right to left patent ductus arteriosus).24 In terms of its effect on oxygenation,. . a shunt differs from venous admix- Step 5: Evaluate Oxygenation ture that occurs from decreased V/Q ratios by being poorly responsive to Hypoxemia refers to a reduction of oxygen in the oxygen supplementation.6 Because shunted blood receives no air from the arterial blood, indicated by Pao values below 80 2 alveoli, increasing the fraction of inspired oxygen (Fio2) does not typically 6 mm Hg. The presence of hypoxemia can be life- improve oxygenation. In contrast, oxygen supplementation may .improve. threatening, and a Pao2 value below 60 mm Hg hypoxemia in patients with venous admixture because the low-V/Q lung warrants immediate therapeutic intervention.4 Any areas are still exchanging some alveolar air. Ultimately, patients that do

time a low Pao2 is obtained from a patient breath- not adequately respond to oxygen supplementation may need mechanical ing room air, the alveolar gas equation should be ventilation in an attempt to reopen and convert collapsed alveoli into more 26 used to determine the alveolar–arterial (a–a) oxy- functional gas exchange units. 6 a gen gradient (see below). Normal values for the Martin L. Pao2 and the alveolar-arterial Po2 difference. In: Martin L, ed. All You Really Need to Know to Interpret Arterial Blood Gases. Baltimore: Lippincott Williams & Wilkins; 1999:55-57. 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, In these equations, PB is atmospheric pressure the a–a oxygen gradient provides a measure of (760 mm Hg at sea level), and 47 is the water the adequacy of oxygen transfer across the alveo- vapor pressure in mm Hg (which is subtracted lar membrane into the pulmonary capillaries per- because only dry alveolar gas pressures are mea- fusing the alveoli (i.e., oxygen loading into the sured). The factor 1.2 represents the respiratory 24,25 blood). Serial calculations of the a–a oxygen quotient, or the ratio of oxygen uptake to CO2 gradient allow for objective estimates of pulmo- exhaled. Figure 1 helps illustrate the concept. nary function over time.24,26 The following equation is a simplified ver- Most pulmonary diseases. .alter the vent- sion of the alveolar gas equation that can be ilation:perfusion ratio (i.e., V/Q mismatch) of used for patients breathing room air (Fio2 = 24 individual alveoli, which leads to a reduction in 0.21) at sea level (PB = 760 mm Hg) : oxygen loading into the blood and a correspond. . - 26 Pa o 2 = 150 – (1.2 × Pac o 2) ing lower Pao2 (Figure 1 and Box 2). V/Q mis- matches lead to an increase in the a–a gradient. The calculations used to quantify pulmonary gas Clinically, a normal a–a gradient (5 to 15 mm exchange efficacy in the presence of hypoxemia Hg) excludes pulmonary disease and suggests

(Pao2 <80 mm Hg) at room air and obtain the a–a that arterial hypoxemia (Pao2 <80 mm Hg) is 4,24 gradient are as follows : due to hypoventilation (increased Pac o 2) or decreased inspired oxygen.26 Patients with a Alveolar gas equation: Alveolar partial pressure of gradient above 25 mm. Hg. should be considered oxygen (Pa o 2) = [Fio2 × (PB – 47)] – (1.2 × Pac o 2) to have a degree of V/Q mismatch from pulmo- nary parenchymal disease, although cardiovas- 17,26 a–a Gradient = Pa o 2 (calculated) – Pao2 (measured) cular pathology can also affect this value.

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FREE CE Blood Gases: Interpretations and Clinical Applications

Conclusion therapeutic interventions. Serial measure- Blood gas analysis helps assess three vital ments can be used to assess proper response physiologic processes in critically ill veterinary to therapy. Blood gas analysis requires a step- patients: acid–base status, ventilation, and oxy- by-step approach and practice. Blood gas data genation. Initial blood gas analysis helps diag- should always be interpreted in light of full nose underlying disease processes and guide clinical and laboratory information. QuickNotes References Ventilation can be 1. Cornelius LM, Rawlings CA. Arterial blood gas and acid–base 13. Wall RE. Respiratory acid–base disorders. Vet Clin North Am Small values in dogs with various diseases and signs of disease. JAVMA Anim Pract 2001;31(6):1355-1367. assessed by Pc o 2 1981;178(9):992-995. 14. Guyton AC, Hall JE. Pulmonary ventilation. In: Textbook of Medical measurements 2. Mathews K. Acid–base assessment. In: Mathews K, ed. Veterinary Physiology. 11th ed. Philadelphia: Elsevier Saunders; 2006:477. Emergency and Critical Care Manual. 2nd ed. Guelph, ON: LifeLearn; 15. Johnson RA. Respiratory acidosis: a quick reference. Vet Clin North from an arterial 2006:406-410. Am Small Anim Pract 2008;38(3):431-434. 3. Ilkiw JE, Rose RJ, Martin IC. A comparison of simultaneously col- sample (Pac o 2) 16. Johnson RA. Respiratory alkalosis: a quick reference. Vet Clin North lected arterial, mixed venous, jugular venous and cephalic venous blood Am Small Anim Pract 2008;38(3):427-430. or Pvc o 2­ from a samples in the assessment of blood-gas and acid–base status in the dog. 17. Bateman SW. Making sense of blood gas results. Vet Clin North Am central venous J Vet Intern Med 1991;5(5):294-298. Small Anim Pract 2008;38(3):543-557. 4. Haskin S. Interpretation of blood gas measurements. In: Lesley KG, 18. de Morais HA. Metabolic acidosis: a quick reference. Vet Clin North sample in patients ed. Textbook of Respiratory Disease in Dogs and Cats. St Louis: WB Am Small Anim Pract 2008;38(3):439-442. Saunders; 2004:181-193. 19. Constable PD. Clinical assessment of acid–base status: compari- with adequate 5. Wingfield WE, Van Pelt DR, Hackett TB, et al. Usefulness of venous son of the Henderson-Hasselbalch and strong ion approaches. Vet Clin blood in estimating acid–base status of the seriously ill dog. J Vet Emerg perfusion. Pathol 2000;29(4):115-128. Crit Care 1994;4(1):23-27. 20. Foy D, de Morais HA. Metabolic alkalosis: a quick reference. Vet Clin 6. Day TK. Blood gas analysis. Vet Clin North Am Small Anim Pract North Am Small Anim Pract 2008;38(3):435-438. 2002;32(5):1031-1048. 21. Autran de Morais HS, Dibartola SP. Ventilatory and metabolic com- 7. Davis H. Arterial and venous blood gases. In: Wingfield WE, Raffe pensation in dogs with acid–base disturbances. J Vet Emerg Crit Care MR, eds. The Veterinary ICU Book. Jackson, WY: Teton NewMedia; 2002:258-259. 1991;1(2):39-49. 8. Ford RB, Mazzaferro EM. Diagnostics and therapeutic procedures: 22. Martin L. Primary and mixed acid–base disorders. In: Martin L, ed. advanced procedures. In: Winkel AJ, ed. Kirk and Bistner’s Handbook All You Really Need to Know to Interpret Arterial Blood Gases. 2nd ed. of Veterinary Procedures and Emergency Treatment. 8th ed. St. Louis: Baltimore: Lippincott Williams & Wilkins; 1999:136-137. Saunders Elsevier; 2006:508-509. 23. Adams LG, Polzin DJ. Mixed acid–base disorders. Vet Clin North 9. Bailey JE, Pablo LS. Practical approach to acid–base disorders. Vet Am Small Anim Pract 1989;19(2):307-326. Clin North Am Small Anim Pract 1998;28(3):645-662. 24. Camps-Palau MA, Marks SL, Cornick JL. Small animal oxygen ther- 10. Haskins SC. An overview of acid–base physiology. JAVMA 1977; apy. Compend Contin Educ Pract Vet 1999;21(7):1-10. 170(4):423-428. 25. Van Pelt DR, Wingfield WE, Wheeler SL, Salman MD. Oxygen-ten- 11. McNamara J, Worthley LI. Acid–base balance: part I. Physiology. sion based indices as predictors of survival in critically ill dogs: clinical Crit Care Resusc 2001;3(3):181-187. observations and review. J Vet Emerg Crit Care 1991;1(1):19-25. 12. Robertson SA. Simple acid–base disorders. Vet Clin North Am 26. Clare M, Hopper K. Mechanical ventilation: indications, goals, and Small Anim Pract 1989;19(2):289-306. prognosis. Compend Contin Educ Pract Vet 2005;27(3):194-208. 3 CE CREDITS CE Test This article qualifies for 3 contact hours of continuing education credit from the Auburn University College of Veterinary Medicine. Subscribers may take individual CE tests online and get real-time scores at CompendiumVet.com. Those who wish to apply this credit to fulfill state relicensure requirements should consult their respective state authorities regarding the applicability of this program.

1. A pH of 7.40 means the a. correlates with a faster respiratory rate d. a negative value always indicates a meta- – a. HCO3 concentration is within normal and an increased respiratory effort. bolic acidosis, not metabolic compensa- limits. b. causes an increase in the a–a gradient. tion for a respiratory alkalosis.

b. Pc o 2 is within normal limits. c. by itself causes the pH and the Pao2 to c. patient does not have an acid–base decrease. 5. Simple acid–base disturbances are disorder. d. is unresponsive to oxygen typically characterized by which of the – d. HCO3 :Pc o 2 ratio is normal. supplementation. following? a. an abnormal pH with Pc o ­ and HCO – con- 4. The BEecf is the most effective parameter 2 3 2. A simple metabolic acidosis is character- centration values changing in opposite to measure the metabolic component of ized by a low pH and a directions (e.g., ↓HCO – and ↑Pc o ) a. decreased BEecf, HCO – concentration, acid–base disorders because 3 2 3 b. an acid–base disorder (metabolic or and Pc o . a. it is the only useful parameter when 2 respiratory in origin) and no apparent – calculating the amount of sodium bicar- b. normal BEecf and HCO3 concentration bonate to administer to severely acidemic change in the opposing system and increased Pc o 2. patients. c. a neutral pH (7.4) with abnormal Pc o 2­ o r c. decreased Tc o 2. – – b. it is a direct measurement, not a HCO3 concentration values d. normal BEecf and HCO3 concentration and decreased Pc o . calculation. d. an acid–base disorder (metabolic or 2 c. it standardizes for the respiratory contri- respiratory in origin) and a quantifiable

3. Hypoventilation (↑Pc o 2) is potentially dan- bution (Pc o 2 of 40 mm Hg) to the acid– parallel compensation in the opposing – gerous because it base balance. system (e.g., ↓HCO3 and ↑Pc o 2)

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FREE Blood Gases: Interpretations and Clinical Applications CE

6. Jack, an adult Labrador retriever, pre- Bonbon’s metabolic alkalosis could be 9. Please explain Lucy’s oxygenation status sented with a 2-day history of weakness, explained by from her arterial blood gas results. The excessive thirst, and urination. On exami- a. an upper GI obstruction with loss of gas- sample was collected before oxygen nation, he was found to be 8% to 10% tric juices in the vomitus. supplementation was instituted. dehydrated. Please explain Jack’s acid– b. pain-associated hypoventilation. base status from his initial venous blood c. compensation for the primary respiratory Arterial blood gas results (Fio2­ = 21%): gas results: acidosis. Reference d. lactic acidosis from shock. Results Interpretation Value* Venous blood gas results: Pco2 mm Hg 62.1 Hypoxemia 95

Reference 8. Please explain the acid–base status Pco2 mm Hg 67.6 Respiratory acidosis 38 Results Interpretation Value* of Lucy, a geriatric dog with a 3-day *midpoint of range pH 7.012 Acidemia 7.4 history of progressive increased respi- The a–a gradient calculation is: ratory effort. On presentation, Lucy’s Pco2 mm Hg 24.2 Respiratory alkalosis 38 Pa o 2 = 150 – 1.2 (Pac o 2) – temperature was 103.6°F (39.8°C), her HCO3 mEq/L 5.4 Metabolic acidosis 22 Pa o = 150 – 1.2 (67.6) respiratory rate was 42 breaths/min, and 2 BEecf mEq/L -26.2 Metabolic acidosis 0 Pa o = 68.9 her rate was 140 bpm. Her physical 2 *midpoint of range examination revealed inspiratory stridor a–a = Pa o 2 – Pao2 The expected respiratory compensation for on auscultation. a–a = 68.9 – 62.1 = 6.8 this metabolic acidosis (within a margin of variance of ±3 mm Hg) can be calculated as Arterial blood gas results Lucy’s respiratory evaluation reveals follows: (Fio2­ = 21%, at sea level): a. hypoxemia secondary to ventilation–per- fusion abnormalities and hypoventilation. Expected Pc o 2 decrease from midpoint ref- Reference – – Results Interpretation Value* b. hypoxemia secondary to hypoventilation erence value = ∆ HCO3 (decrease in HCO3 concentration from a midpoint reference pH 7.2 Acidemia 7.4 only. c. hypoxemia secondary to ventilation– value associated with the metabolic acidosis) Pco mm Hg 62.1 Hypoxemia 95 2 perfusion abnormalities only. × 0.7 (expected mm Hg decrease in Pc o 2 for Pco mm Hg 67.6 Respiratory acidosis 38 – 2 d. hypoxemia secondary to pulmonary each 1.0 mEq/L decrement in HCO3 ) – HCO3 mEq/L 30.4 Metabolic alkalosis 22 disease. In this case: (22 – 5.4) × 0.7 BEecf mEq/L +12.4 Metabolic alkalosis 0 16.6 × 0.7 = 11.6 mm Hg *midpoint of range 10. Bob is a young adult mixed-breed dog that presented after being hit by a car. The expected metabolic compensation for Expected Pco2 = Pco2 midpoint reference Physical examination revealed extensive range – Expected change in Pco2 this chronic respiratory acidosis (within a abrasions on his thorax. His temperature margin of variance of ± 2 mEq/L) can be cal- was 102.8°F (39.4°C), his respiratory rate In this case: culated as follows: was 62 breaths/min, and his heart rate 38 mm Hg – 11.6 = 26.4 mm Hg was 140 bpm. Please explain Bob’s oxy- – Expected HCO3 increase from midpoint Therefore, Jack’s expected Pco2 is 26.4 mm genation status from the arterial gas data reference value = ∆ Pc o 2 (increase in Pc o 2 Hg, and his measured Pco2 is 24.2 mm Hg. collected on presentation: from midpoint reference range associ- ated with the respiratory acidosis) × 0.35 Arterial blood gas results (Fio ­ = 21%): After reviewing Jack’s measured and – 2 (expected mEq/L increase in HCO3 for expected Pco2 values, we can conclude Reference each 1.0 mm Hg increment in Pc o ): that Jack’s respiratory compensation for 2 Results Interpretation Value* his metabolic acidosis is In this case: (67.6 – 38) × 0.35 pH 7.48 Alkalemia 7.4 a. adequate (within the ±3 margin of 29.6 × 0.35 = 10.4 mEq/L Pco mm Hg 63 Hypoxemia 95 variance). 2 Pco mm Hg 25.9 Respiratory alkalosis 38 b. inadequate (outside the ±3 margin of Expected HCO – = HCO – midpoint reference 2 3 3 – – HCO3 mEq/L 18.8 Metabolic acidosis 22 variance). range + Expected increase in HCO3 c. acute. BEecf mEq/L -4.8 Metabolic acidosis 0 d. chronic. In this case: *midpoint of range 22 + 10.4 = 32.4 mEq/L The a–a gradient is: 7. Bonbon, a shih tzu puppy, presented with a Therefore, Lucy’s expected HCO – is 32.4 Pa o 2 = 150 – 1.2 (Pac o 2) 2-day history of vomiting and anorexia. On 3 mEq/L, and her measured HCO –­ is 30.4 Pa o 2 = 150 – 1.2 (25.9) physical examination, a foreign body was 3 Pa o 2 = 119 palpated in the cranial abdomen. Please mEq/L.

explain Bonbon’s acid–base status from a–a = Pa o 2 – Pao2 her initial venous blood gas results: Lucy’s acid–base status can be described a–a = 119 – 63 = 56 as Venous blood gas results: a. a mixed acid–base disorder. Bob’s respiratory evaluation reveals b. respiratory acidosis with adequate meta- a. hypoxemia secondary to ventilation–per- Reference bolic compensation (within the Results Interpretation Value* fusion abnormalities and hypoventilation. ±2 margin of variance). b. hypoxemia secondary to hypoventilation pH 7.5 Alkalemia 7.4 c. metabolic alkalosis with respiratory only. Pco mm Hg 52.1 Respiratory alkalosis 38 2 compensation. c. hypoxemia secondary to ventilation– – HCO3 mEq/L 37.3 Metabolic alkalosis 22 d. respiratory acidosis with no com- perfusion abnormalities only. BEecf mEq/L +12.0 Metabolic alkalosis 0 pensation (outside the ±2 margin of d. hypoxemia secondary to decreased *midpoint of range variance). inspired oxygen.

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