Small Animal Oxygen Therapy

Vol. 21, No. 7 July 1999

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20TH ANNIVERSARY

Refereed Peer Review

FOCAL POINT

Small Animal Oxygen Therapy

★ Oxygen (O ) therapy optimizes 2

blood O2 content, helps increase O2 delivery to tissue, and decreases the ventilatory and myocardial work necessary to maintain adequate tissue oxygenation.

KEY FACTS ■ The five causes of hypoxemia are low fraction of inspired O2 (FIO2), hypoventilation, diffusion barrier impairment, shunt, and ventilation/perfusion mismatch. ■ As a general rule, the delivered O2 concentration should not exceed an FIO2 of 50% for more than 24 hours or complications associated with O2 toxicity may develop. ■ Delivered O2 should be humidified when supplementation is required for more than a few hours or if the upper respiratory airways are bypassed. ■ Arterial blood gas analysis, alveolar–arterial O2 tension difference, arterial partial pressure of O2:FIO2 ratio, and pulse oximetry are ancillary tests that support the need for and help to monitor response to O2 therapy.

Louisiana State University

Maria A. Camps-Palau, DVM Steven L. Marks, BVSc, MS, MRCVS Janyce L. Cornick, DVM, MS ABSTRACT: Oxygen (O2) therapy is easy to administer, readily available, and relatively safe if used judiciously. Optimizing O2 delivery to tissue is imperative in clinical conditions characterized by hypoxia. It is important to understand the physiology of O2 uptake and delivery to recognize those patients that will benefit from O2 supplementation. Several O2 administration techniques are available and can be adapted to every clinical situation and patient condition. O2 therapy is an important adjunctive therapy but is not without complications and thus must be closely monitored.

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ypoxia is a broad term that means decreased levels of oxygen (O2) in air, blood, or tissue.1 Clinically, hypoxia is defined as inadequate supply of O2 to the body’s tissue and can result from insufficient blood oxygenation (i.e., hypoxemia), reduced O2-carrying capacity of erythrocytes, decreased tissue blood flow, increased tissue demand for O2, or impaired tissue extraction of O2.2,3 Oxygen is easy to administer, readily available, and relatively safe. Supplementation with O2 increases blood O2 content, minimizes detrimental effects of hypoxemia, and decreases ventilatory and myocardial work necessary to maintain tissue O2 delivery.4,5 Therapeutic considerations in animals with abnormalities that increase O2 demand or decrease O2 delivery to tissue include correction of the underlying problem and maintenance of adequate tissue oxygenation. When evaluating patients that may benefit from O2 therapy, understanding respiratory and O2-transport physiology is necessary to formulate a rational diagnostic and therapeutic plan. When O2 delivery to tissue is inadequate, cells must use alternate anaerobic pathways to maintain their metabolism. Anaerobic metabolism causes rapid depletion of energy and accumulation of lactic acid within cells, leading to cellular dysfunction and death.4,6 This article discusses the physiology of respiration and O2 uptake and delivery, indications for O2 supplementation, methods of O2 administration, and criteria to assess response to O2 therapy.

RESPIRATORY PHYSIOLOGY The major function of the respiratory system is to exchange O2 and carbon

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Hemoglobin Saturation (SO2; %)

dioxide (CO2) between blood PHYSIOLOGY OF Arterial Oxygen Content Formula and inspired air to maintain OXYGEN UPTAKE normal arterial partial pres- CaO2 = Oxyhemoglobin + Dissolved O2 AND DELIVERY sures of O2 (PaO2) and CO2 CaO (ml O /dl) = Oxygen is carried in the 2 2 (PaCO2). The O2 pathway can blood in either the dissolved (SaO2 [%] × Hemoglobin [g/dl] × 1.34 [ml O2/g]) + be divided into four major state or bound to hemoglo(PaO2 [mm Hg] × 0.003 [ml O2/dl/mm Hg]) functions—pulmonary gas bin (oxyhemoglobin).2,4 Arteexchange, diffusion of gases CaO2 = arterial oxygen content; O2 = oxygen; PaO2 = arterial rial O2 content (CaO2) is the between alveoli and blood, partial pressure of oxygen; SaO2 = arterial hemoglobin amount of oxyhemoglobin transport of gases to and from saturation. plus the O2 dissolved in plascells, and regulation of ventima (see Arterial Oxygen lation.2,4 Content Formula).6 The contribution of dissolved O2 to Despite the variable demands of the body, the respioverall CaO2 is relatively small because most O2 travels as ratory control system maintains PaO2 and PaCO2 within oxyhemoglobin.2,4 Tissue hypoxia can result from dea narrow homeostatic range. The basic components of creased CaO2 even in patients that maintain normal the respiratory control system are the central and pePaO2 values. Causes of decreased CaO2 include anemia ripheral chemoreceptors, medullary respiratory center, and hemoglobin abnormalities.2,4 2 and muscles of respiration. Under normal conditions, The sigmoid shape of the oxyhemoglobin dissociathe primary driving forces for alveolar ventilation are tion curve (Figure 1) demonstrates that the amount of hypercapnia (sensed by the central chemoreceptors in O2 bound to hemoglobin increases rapidly up to a parthe brain stem) and, to a lesser degree, hypoxemia tial pressure of O2 (PO2) of approximately 50 mm Hg; (sensed by the peripheral chemoreceptors in the aortic however, the rate of O2 uptake decreases at higher PO2 arch and carotid bodies).2,4 values. Arterial hemoglobin saturation (SaO2) at a PaO2 The respiratory system consists of the anatomic dead of 100 mm Hg is 97.5%, whereas mixed venous blood space and the respiratory zone. The anatomic dead space with a PO2 of 40 mm Hg has a hemoglobin saturation (i.e., respiratory airways) includes the upper airways and a (SO2) of approximately 75%.2,4 series of branching tubes from the trachea to the termiThe plateau portion of the oxyhemoglobin dissocianal bronchioles that lead inspired air to the gas-exchangtion curve illustrates that a decrease in PaO2 results in ing regions of the lungs. The respiratory zone (i.e., alveominimal changes in the oxygenation of erythrocytes. In lated regions) of the lungs is where gas exchange occurs. contrast, the steep lower part of the curve indicates that Alveolated regions that are ventilated but not perfused small drops in capillary PO2 allow peripheral tissue to constitute the physiologic dead space.2,4 receive large amounts of O2 from erythrocytes. At the blood–gas interface, the pulmonary capillaries A right shift of the oxyhemoglobin dissociation curve form a dense network in the decreases the affinity of hemoalveolar walls and have diameglobin for O2, thereby facilitatters just large enough for a sining O2 release because a higher Plateau Phase gle erythrocyte to pass.2 The PaO2 is necessary to load hemo100 rate and direction of gas moveglobin with O2. Right shifts are ment are based on pressure seen with acidosis (Bohr effect), 75 gradients and follow Fick’s law, hypercapnia, hyperthermia, or which states that the amount increases in erythrocyte 2,3of gas moving through a sheet diphosphoglycerate (2,3-DPG) 50 of tissue is proportional to the concentration.2,4 A left shift of Steep Phase area of that sheet and inversely the curve increases the affinity 25 proportional to its thickness.2 of hemoglobin for O2, which The blood–gas barrier commeans the PaO2 must drop lowprises a large surface area of er for hemoglobin unloading of 25 50 75 100 capillaries wrapping around O2 to occur. Left shifts occur the alveoli and is extremely with alkalosis, hypocapnia, hyOxygen Tension (PO2; mm Hg) thin, thus maximizing exchange pothermia, methemoglobineof O2 and CO2 between alveoli Figure 1—The oxyhemoglobin dissociation curve dem- mia, or 2,3-DPG deficiency.2,4 and capillary blood by simple onstrates the relationship between partial pressure of oxyAccording to Fick’s law, O2 gen and hemoglobin saturation. diffusion.2,4 and CO2 move between sysRESPIRATORY SYSTEM ■ FICK’S LAW ■ OXYHEMOGLOBIN DISSOCIATION CURVE

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temic capillary blood and cells by simple diffusion just as they move between the pulmonary capillary blood and alveolar gas in the lungs.2 O2 delivery is defined as the amount of O2 delivered to a peripheral tissue each minute and is the product of CaO2 and cardiac output.2,4 O2 delivery can be maintained in patients with low CaO2 by increasing cardiac output, assuming cardiac function is normal.2,4 O2 utilization is the amount of O2 consumed by tissue per minute and can be calculated by determining the difference between arterial and venous O2 contents.2,4 Some toxic substances interfere with the ability of tissue to use available O2; an example is cyanide, which prevents the use of O2 by cytochrome oxidase. In this case, the O2 concentrations of arterial and venous blood are high and the O2 utilization by the tissue is extremely low.2

PATHOPHYSIOLOGY OF HYPOXEMIA Arterial partial pressure of O2 is considered abnormally low if its value is less than 75 mm Hg, which at 37˚C, corresponds to an SaO2 of approximately 95%.2,7 Because of the shape of the oxyhemoglobin dissociation curve, PaO2 levels of 60 to 75 mm Hg maintain adequate hemoglobin saturation and whole blood O2 content under normal conditions.5,8 A PaO2 below 60 mm Hg causes stress to a patient,8,9 and subsequent reductions in PaO2 will lead to significant decreases in oxyhemoglobin.8–10 Inadequate blood oxygenation may result from a low fraction of inspired O2 (FIO2), hypoventilation, diffusion impairment, shunt, or ventilation/perfusion (V/Q) mismatch.2,4 Hypoxemia caused by low FIO2 has been associated with anesthetic equipment failure or malfunction, nitrous oxide use, and high altitude.3,9–11 Hypoventilation occurs when there is inefficient gas exchange between the atmospheric air and the alveoli.4 Causes of hypoventilation include those related to central respiratory depression and abnormalities affecting the respiratory apparatus.9,12 Central nervous system (CNS) depression has been associated with CNS and cervical spinal cord trauma; anesthetic drug overdose; and tumors, granulomas, or abscesses of the brain.9,12 Respiratory apparatus abnormalities include upper airway occlusion, bronchial spasm (e.g., anaphylaxis, asthma), pleural space disease (e.g., pneumothorax, pleural effusion, flail chest), thoracic pain, severe abdominal distention (e.g., gastric dilation, ascites), and neuromuscular disease (e.g., myasthenia gravis, botulism, tetanus, organophosphate toxicity).10,11,13,14 Hypoventilation-induced hypoxemia may be alleviated by O2 supplementation, but ventilatory support and correction of the underlying cause are necessary to reestablish eucapnia.4,15–17

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Impaired gas exchange results in a PaO2 that is substantially lower than the PO2 in the alveoli2,4; ventilatory compensation by the respiratory control system usually maintains normal or even decreased PaCO2 during such conditions. 4 The three basic mechanisms of gas exchange impairment are diffusion barrier impairment, shunt, and V/Q mismatch.2,4,9 Diffusion barrier impairment is caused by pulmonary diseases that decrease the area or increase the thickness of the alveolar–arterial membrane, such as interstitial pulmonary edema, pulmonary interstitial fibrosis, and chronic emphysema.18,19 The physiologic efficiency of the lungs makes true diffusion barrier impairment an uncommon cause of hypoxemia because pathologic changes must be very advanced to significantly decrease PaO2.9 This disorder is highly responsive to O2 supplementation.9 Shunt occurs when venous blood bypasses gas-exchange areas of the lungs and mixes with oxygenated arterial blood (venous admixture). This cause of hypoxemia accompanies many types of lung diseases, such as right-to-left cardiac shunt, pneumonia, cardiogenic and noncardiogenic alveolar pulmonary edema, and lung atelectasis.2 Shunts are typically poorly responsive to O2; however, in patients with severe hypoxemia, small increases in PaO2 may significantly increase blood O2 content and hence peripheral O2 delivery.19 This occurs because, at extreme degrees of shunting, PaO2 values correlate to the rapidly changing portion of the oxyhemoglobin dissociation curve.19 Ventilation/perfusion mismatch occurs when alveolar ventilation and blood flow are not closely matched; this results in inefficient gas exchange and hypoxemia.2,4 V/Q mismatch is a frequent cause of hypoxemia in animals with pulmonary thromboembolism, acute respiratory distress syndrome, alveolar pulmonary edema, pulmonary contusions, pulmonary neoplasia, and pneumonia.10,14,17–19 A high V/Q mismatch (e.g., pulmonary thromboembolism) is seen when regions of the lung are ventilated but not perfused, causing an increase in the physiologic dead space of the lung; patients with high V/Q mismatches typically respond well to O2 supplementation.2,4,6 In contrast, a low V/Q mismatch (e.g., pulmonary contusion) occurs when regions of the lung are perfused but not ventilated; the functional result is a pulmonary shunt. Low V/Q mismatches respond poorly to O2 therapy.2,4,6

INDICATIONS Oxygen therapy is indicated in patients with clinical conditions associated with hypoxia (see Indications for Oxygen Therapy). Hypoxia is caused by hypoxemia, decreased tissue blood flow, reduced O2-carrying capac-

OXYGEN DELIVERY ■ FRACTION OF INSPIRED OXYGEN ■ VENTILATION/PERFUSION MISMATCH

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ity of erythrocytes, or increased deIndications for Oxygen Therapy mand for O2 by tissue.2–4,9–14 Diminished O2 delivery to tissue occurs in Hypoxemia cases of generalized decreased tissue blood flow (e.g., congestive heart Low fraction of inspired oxygen Diffusion impairment failure, shock, cardiopulmonary Anesthesia accident Interstitial pulmonary edema arrest) or local vascular obstrucHigh altitude Pulmonary interstitial fibrosis tion.20,21 Anemia and hemoglobin Chronic emphysema abnormalities (e.g., carboxyhemoVentilation/perfusion mismatch globinemia, methemoglobinemia) Pulmonary thromboembolism Hypoventilation reduce the ability of hemoglobin to Acute respiratory distress 22–24 Central nervous system depression Increased tissue O2 decarry O2. syndrome Upper airway obstruction mand occurs in hyperthermia (e.g., Alveolar pulmonary edema Bronchial spasm (anaphylaxis) fever, heat stroke, malignant hyper3,25–27 Pulmonary contusion Pleural filling defect thermia), sepsis, and seizures. Pulmonary neoplasia Thoracic pain Clinical signs of hypoxia include Pneumonia cyanosis, tachypnea, dyspnea, tachyAbdominal distention cardia, psychomotor incoordinaNeuromuscular disease Shunt tion, gastrointestinal upset, and restRight-to-left cardiac shunt lessness.10,11,13,14 Although cyanosis Atelectasis indicates the need for O2 therapy, at least 5 g/dl of deoxygenated hemoDecreased oxygen delivery globin in the circulating blood is necessary for it to be apparent.2,4,10 Reduced blood flow Anemia Patients suffering from anemia or Congestive heart failure carbon monoxide poisoning may Hemoglobin malfunction Cardiovascular shock not appear cyanotic but will usually Carboxyhemoglobin Vascular obstruction benefit from O2 therapy.28,29 AncilMethemoglobin lary tests, such as arterial blood gas analysis, pulse oximetry, and alveoIncreased oxygen demand lar–arterial O 2 tension difference (i.e., A-a gradient), help support the Hyperthermia Sepsis presence of hypoxemia or hypoxia.3 Fever Oxygen therapy is beneficial in Seizures Heat stroke treating patients with craniocerebral Malignant hyperthermia trauma,10,11,13,30–33 which may experience cerebral ischemia caused by inHead trauma creased intracranial pressure and subsequent reduction in cerebral perIn most clinical situations, an FIO2 of 30% to 40% fusion. This results in increased cerebral PCO2 and decreased cerebral PO2, which cause an increase in cerebral provides adequate hemoglobin saturation and is considblood flow and further increases in intracranial presered safe.34,35 As a general rule, the delivered O2 concen30,32,33 Although hyperventilation has been the major tration should not exceed 50% for more than 24 hours sure. therapeutic approach to craniocerebral trauma patients, or complications associated with O2 toxicity may develop.2,34,36 However, patients should not be deprived of O2 supplementation is essential to ensure adequate cere31–33 bral O2 delivery. higher concentrations of O2 if necessary to maintain an adequate PaO2, especially during the initial stabilization OXYGEN ADMINISTRATION TECHNIQUES period.2,34,36 If 100% inspired O2 fails to increase the Several techniques for O2 supplementation are availPaO2 to a minimum of 60 mm Hg or if the PaCO2 is able. Selection of the appropriate delivery method deunacceptably high, mechanical ventilatory support pends on the animal’s primary problem, desired FIO2, must be incorporated into the therapeutic plan.8,15,16 Humidification is recommended when O2 suppleanticipated treatment duration, available equipment, mentation is delivered for more than a few hours and is and patient size and temperament. ANCILLARY TESTS ■ CRANIOCEREBRAL TRAUMA ■ OXYGEN CONCENTRATION

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particularly important when mately 2 cm from a patient’s the upper respiratory tract is nose creates an area of inbypassed (e.g., O2 delivery creased O 2 concentration via intratracheal catheter or around the animal’s muztracheostomy tube). 10,11,36 zle.37 Although wasteful, this Administration of dry gases technique offers the advandehydrates mucosae, intage of being an easy method creases mucosal secretion for immediate O2 administration and is well tolerated viscosity, degenerates respiby most patients (Figure 3). ratory epithelium, impairs Clinical studies have shown mucociliary apparatus functhat O2 flow rates of 2 to 3 tion, and increases the risk of infection.4,11 Humidifica- Figure 2—The face mask technique is used for emergencies L/min can achieve an FIO2 of 25% to 40%.37 tion can be accomplished by and short-term oxygen administration. delivering O2 through a polyElizabethan Collar ethylene tube submerged in Canopy a bottle partially filled with The Elizabethan collar sterile saline solution. The canopy is created by placing humidified O 2 from the space above the solution is an Elizabethan collar snugly collected by a second polyaround the neck and securethylene tube and delivered ing an O2 line along the animal’s neck, with the tip to the patient. placed inside the collar. The Face Mask front of the collar is then Oxygen administration via covered with cellophane, and a face mask is well suited for a small vent hole is made in short-term O 2 delivery in the cellophane to help elimemergency situations and inate the warm, humid exfor evaluation of the effecpired air (Figure 4). The tiveness of supplemental O2 Figure 3—The flow-by technique provides emergency oxygen FI O 2 achieved inside the in equivocal cases. Tank O2 administration for critically ill, stressed patients. canopy depends on a variety regulated through a flow of factors, including the meter may be used as an O2 source. Alternatively, an tightness of the collar, size of the vent hole, size of the anesthetic machine with either a circle rebreathing syspatient, and respiratory rate. Although this method is tem or nonrebreathing circuit can provide a method for effective, economic, and easy to set up, disadvantages O2 delivery. The nonrebreathing circuit allows CO2 reinclude O2 leakage, hyperthermia, high humidity, CO2 retention, and lack of patient cooperation. Clinical moval if adequate O2 flow is used. Ophthalmic ointment should be applied periodically to prevent corneal studies in healthy, anesthetized dogs using an O2 flow rate of 0.75 to 1 L/min have documented an FIO2 of desiccation. The face mask technique can be initiated 30% to 40%.38 In clinical situations, however, an iniimmediately, requires minimal set up and equipment, is tially high O2 flow rate is recommended to quickly fill easy to use, and allows convenient access to patients. the canopy with O2, followed by an O2 flow rate of 2 to Many animals may not tolerate the mask, and constant 5 L/min to ensure adequate O2 delivery. supervision is required (Figure 2). Clinical studies in healthy, anesthetized dogs using well-fitting masks with Nasal Catheter Delivery an O2 flow rate of 0.5 L/min have documented an FIO2 of 40% to 50%.37 However, a loose-fitting mask and an To use a nasal catheter O2 delivery system, topical O2 flow rate of 2 to 5 L/min will ensure minimal reanesthetic (e.g., 2% lidocaine, proparacaine) is instilled breathing of exhaled CO2 and entrainment of room air into one nostril and a lubricated, soft rubber catheter if needed to meet peak inspiratory demands of the patient. (5 to 10 Fr, depending on the size of the animal) with multiple fenestrations at the distal end is introduced Flow-By through the naris into the ventral meatus. The catheter Holding the end of an O2 delivery source approxiis advanced to the level of the carnassial tooth, and the HUMIDIFICATION ■ NONREBREATHING CIRCUIT ■ FLOW RATES

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remainder is attached to the attached to a humidified O2 source.39 This method is indorsum of the nose and head expensive, efficient, and well with sutures or an adhesive tolerated; provides continuagent (e.g., cyanoacrylate).35 To avoid inflammation of ous O2 administration; and the mucosa, nasal catheters allows easy access to the pashould be changed every 24 tient. Intratracheal catheters to 48 hours and replaced in are invasive and more diffialternate naris.35 cult to place than are inThis mode of O2 administranasal catheters and, altration allows free access to though less irritating than the patient and is one of the nasal catheters, have been most efficient, convenient, associated with tracheitis.36,39 Other potential disadvancost-effective, and well-tolerated methods available Figure 4—The Elizabethan collar canopy is used for tempo- tages include kinking of the catheter at the skin entry (Figure 5). Nasal catheteri- rary oxygen therapy. site and subcutaneous insufzation is primarily used for flation of O2 caused by cathprolonged O 2 therapy, but ease of application makes it eter misplacement. An O 2 flow rate of 50 ml/kg/min a suitable short-term option has been recommended to for animals that will not tolachieve an FIO2 of 40% to erate a face mask. The FIO2 achieved by this method 60%.36 varies considerably dependOxygen Cage ing on the patient’s size, resThe oxygen cage method piratory rate, and extent to of delivery requires a sealed which the animal is mouth compartment with mechabreathing. Disadvantages innisms to regulate O2 concenclude serous nasal discharge tration and ambient temproduction, jet damage perature and humidity as (caused by high flow of O2) to the nasal mucosa, and Figure 5—The nasal catheter delivery system is suitable for well as to eliminate expired lack of patient tolerance. In prolonged oxygen therapy. CO2. This is a noninvasive system that allows accurate one report, a small dog demonitoring and control of veloped signs of gastric dilathe environment (Figure 6). Major disadvantages intion secondary to high O2 flow rates.35 An O2 flow rate of 0.75 L/min reportedly produces an FIO2 of 30% to clude expense, O2 waste, and isolation of the patient 70% in healthy, anesthetized dogs.38 In clinical situafrom the clinician. Ambient temperature should be tions, O2 flow rates of 100 to 150 ml/kg/min have been maintained at 22˚C (70˚F) with a relative humidity of recommended to achieve an FIO2 of 30% to 50%.35,36 40% to 50%.10,13 It is generally difficult to maintain FIO2 concentrations greater than 40% to 50% when using Intratracheal Catheter Delivery an oxygen cage.10,13 The area over the cricothyroid ligament, or the area Mechanical Ventilation between two tracheal rings in larger dogs (i.e., those Ventilatory support is indicated in the presence of weighing more than 10 kg [20 lb]), is clipped and surhypoventilation, high FIO2 requirements for extended gically prepared for intratracheal catheter placement. periods, respiratory fatigue or arrest, comatose states, Local anesthesia of the skin is recommended, and asepand increased intracranial pressure as well as when pastic technique must be followed. A large-gauge, long, sive O 2 delivery fails to adequately correct hypoxflexible catheter with a fenestrated distal end is inserted emia.15,16,30,31 A review of ventilatory techniques, such as via a large-bore needle; the needle is withdrawn; and positive end-expiratory pressure ventilation, continuous the catheter is advanced until the tip lies just cranial to positive-pressure ventilation, and intermittent positivethe carina (at approximately the fifth intercostal space). pressure ventilation, may be found in the literature.15,16 The catheter is secured in place with a neck wrap and JET DAMAGE ■ TRACHEITIS ■ VENTILATORY SUPPORT

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ing a precise FI O 2 may be MONITORING difficult with some methods RESPONSE TO THERAPY of O2 delivery. In humans, Arterial blood gases and the Pa O 2:FI O 2 ratio should pulse oximetry are used to asbe greater than 300 in norsess pulmonary function and mal patients breathing room the patient’s response to O2 air.40,41 We consider a PaO2: supplementation and to help FIO2 ratio greater than 200 determine the lowest concensuggestive of a positive retration of O 2 delivery that sponse to O2 supplementaprevents hypoxemia. Calcution.41 Values for PaO2:FIO2 lated A-a gradients and ratio less than 100 suggest Pa O 2:FI O 2 ratios are useful poor response to O2 therapy.40,41 tools to estimate the gas-exPulse oximetry, which dischange efficiency of the Figure 6—The oxygen cage provides a controlled environ- plays SaO and pulse rate vallungs.2,3,19 2 ues, provides objective asBlood gas analysis is the ment and is suitable for prolonged oxygen therapy. sessment of the need for O2 most accurate method to supplementation and can be used to continuously monmeasure the degree of hypoxemia.9,19 Arterial blood gas itor a patient during O2 administration.3,42 Although analysis measures the amounts of O2 and CO2 in arteriSaO2 is not linearly related to PaO2, it is an indirect meaal blood, reflecting the functional efficiency of the sure of PaO2. As illustrated by the oxyhemoglobin dissolungs and response to O2 therapy.9 Major disadvantages ciation curve, SaO2 provides information about delivery of this analysis are difficulty in obtaining arterial blood of O2 to tissue.3,9,19,42 Factors that interfere with accurate samples and availability and cost of the necessary tech3,9 SaO2 readings include tissue thickness and pigmentation, nology. In healthy animals breathing room air (FIO2, decreased tissue perfusion, hypothermia, bilirubinemia, 21%), values for PaO2 and PaCO2 are 90 to 100 mm Hg anemia, and motion.3,42 Advantages of this method comand 35 to 45 mm Hg, respectively.3,9 pared with blood gas analysis include continuous, imThe A-a gradient is calculated from arterial blood gas mediate, and noninvasive estimation of blood oxygenaanalysis and is a sensitive measure of gas-exchange effition.42 Transmission probes can be placed on the digits, ciency (see Alveolar–Arterial Gradient Formula).2,19 The tongue, lips, or other nonpigmented mucous memA-a gradient formula allows clinicians to estimate the branes; reflectance probes are placed in the esophagus or adequacy of O2 transfer from the alveolus to the pulrectum, increasing the versatility of SaO2 monitoring.3 monary capillary blood in animals breathing room air at Pulse oximetry can be used in conjunction with arterial sea level. If the lung is perfectly homogeneous, there blood gas measurements in critical patients to reduce should be no difference between the calculated A-a grathe number of blood samples needed.3 In the absence of dient and the measured PaO2; any factor making gas exarterial blood gas analysis, the limitations of pulse change less efficient will lead to a widening of the A-a oximetry must be recognized.3,42 gradient.19 The A-a gradient should be less than 10 mm 9 Clinical response to O2 administration provides an Hg in normal animals breathing room air. An A-a graadequate evaluation of therapeutic efficacy in the abdient of 15 mm Hg is indicative of decreased oxygenatsence of ancillary tests. Patients benefiting from O2 ing efficiency of the lungs (venous admixture).2,9 Values therapy should show imgreater than 30 mm Hg sugproved mucous membrane gest clinically significant imAlveolar–Arterial (A-a) Gradient Formula color, decreased heart rate, pairment of gas exchange and decreased respiratory rate the need for additional O 2 A-a gradient = P O – PaO A 2 2 and effort, and reduced anxisupplementation.9 = (FIO2 × [PB – PH2O] – 1.2 × PaCO2) – PaO2 ety.10,13 Gas-exchange abnormali= (0.21 × [760 – 47] – 1.2 × PaCO2) – PaO2 Analyzing arterial blood ties can also be reflected in gases and pulse oximetry the PaO2:FIO2 ratio.40,41 This = (150 – 1.2 × PaCO2) – PaO2 recorded while an animal is ratio provides an assessment of gas exchange similar to the FIO2 = fraction of inspired oxygen; PAO2 = alveolar partial breathing room air may help pressure of oxygen; PaO2 = arterial partial pressure of monitor progress and deterA-a gradient and is more eas- oxygen; PaCO = arterial partial pressure of carbon dioxide; 2 mine the ongoing need for ily calculated from blood gas PB = barometric pressure; PH2O = vapor pressure of water. therapy.8,9 Discontinuation of analysis40; however, determinP a O 2: F I O 2 R A T I O ■ P U L S E O X I M E T R Y ■ C L I N I C A L R E S P O N S E

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Announcing a new forum for timely publication of research results— Veterinary Therapeutics: Research in Applied Veterinary Medicine. A quarterly journal dedicated to rapid publication, Veterinary Therapeutics invites the submission of clinical and laboratory research manuscripts in small and large animal medicine, including pathophysiology, diagnosis, treatment, and prognosis. Prospective, retrospective, and corroborative studies are all welcome. Accepted articles are scheduled to be published 90 to 120 days after submission. Contact Toni Passaretti, 609-671-2022, email [email protected].

Another fine publication from the publisher of Compendium.

COMPLICATIONS OF OXYGEN THERAPY In patients with long-standing respiratory disease and accompanying chronic hypercapnia, O2 supplementation may occasionally suppress the respiratory drive. Hypoxemia becomes the main stimulus for ventilation in these animals because the sensitivity of the central chemoreceptors for hypercapnia is lost. In these patients, positivepressure ventilation may be required in addition to O2 supplementation while attempts are made to diagnose and treat the underlying cause; however, the prognosis for this type of condition is generally poor.6,17 Prolonged O2 therapy has been associated with suppression of erythropoiesis, pulmonary vasodilation, and systemic arteriolar vasoconstriction.34,36 In dogs, microscopic changes and initial signs of pulmonary dysfunction develop within 24 hours of constant exposure to 100% O2, with additional ENDIU MP exposure to 100% O 2 resulting in death from respiratory failure in 2 to 3 days.34 ANNIVERSARY Inspiration of 30% to 50% O2 does not cause permanent changes, but there is some evidence of increased An increase in the number of permeability of the alveolar facilities that are able to and bronchiolar epithelia.43 administer oxygen therapy plus Conversely, brain malacia the emergence of noninvasive from hypoxemia reportedly and affordable advanced occurs before the onset of monitoring equipment have lung damage induced by made oxygen supplementation a prolonged exposure to high useful and practical therapeutic O2 tensions.30,33,34 The most tool for general practitioners. prudent approach to O 2 Another important contribution supplementation is to use to the increasing awareness and the lowest possible FI O 2 management of critically ill pets necessary to provide an adis the recognition and equate beneficial effect. S
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I Are you involved in research?

O2 therapy should be based on improvement of clinical signs and resolution of the primary disease. It is recommended that patients be slowly weaned off O2 over 24 to 48 hours, using blood gas analysis and pulse oximetry for objective evaluation.11,13

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promotion of emergency and critical care medicine as a specialty within veterinary medicine. (Photo: Drs. CampsPalau [left] and Marks.)

SUMMARY Oxygen therapy is easy to administer, readily available, and relatively safe if used judiciously. Optimizing O2 delivery to tissue is imperative in a number of clinical conditions in which hypoxia plays an important

DISCONTINUING THERAPY ■ PROLONGED THERAPY

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role. It is important to understand the physiology of O2 uptake and delivery to recognize patients that will benefit from O2 supplementation. Several techniques for O2 administration are available and can be adapted to specific clinical situations and patient conditions. O2 therapy is an important adjunctive therapy but is not without complications and must be used judiciously. Arterial blood gases, A-a gradients, PaO2:FIO2 ratio, and pulse oximetry are used to assess patient response to O2 supplementation and help determine the lowest concentration of O2 delivery that prevents hypoxemia. In the absence of ancillary tests, clinical evaluation of the patient is an appropriate diagnostic tool to assess response to O2 and monitor cessation of therapy. As a guideline for prolonged supplementation of O2, administration of 40% to 50% O2 is generally safe, but patients should not be deprived of higher concentrations of O2 if necessary to maintain adequate PaO2.36 Continual patient assessment is essential; with resolution of the primary problem, O2 therapy may be discontinued gradually.

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ACKNOWLEDGMENTS

The authors thank Dr. Jamie Williams for his encouragement and critique of the manuscript and Dr. Giselle L. Hosgood for her help with the figures.

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About the Authors Drs. Camps-Palau, Marks, and Cornick are affiliated with the Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana. Drs. Marks and Cornick are Diplomates of the American College of Veterinary Internal Medicine; Dr. Cornick is also a Diplomate of the American College of Veterinary Anesthesiologists.