Materials and Methods

Foals—For the investigation, 9 healthy neonatal foals from Iowa State University's teaching herd were used. Each foal was considered healthy on the basis of physical examination findings, adequate passive transfer of maternal antibodies (plasma immunoglobulin concentration at 24 hours after birth, ≥ 800 mg/dL), and the absence of any disorders in the dam during pregnancy or parturition. The duration of gestation in all foals was considered normal. Breeds included Thoroughbreds (n = 5) and Quarter Horses and related breeds (4). There were 5 fillies and 4 colts. The foals’ ages ranged from 3 to 5 days (mean ± SD age, 3.9 ± 0.5 days), and weights ranged from 55 to 67 kg (mean weight, 60.4 ± 3.8 kg). The study protocol was approved by the Iowa State University Animal Care and Use Committee.

Instrumentation—On the day of the experimental procedure, each foal was weighed, a physical examination was performed, and rectal temperature, heart rate, and respiratory rate were recorded. The haired skin over the left dorsal metatarsal artery was clipped and prepared aseptically for catheter placement. A local anesthetic cream^a was applied liberally in the region of the dorsal metatarsal artery at least 10 minutes prior to catheter placement. The foal was sedated with diazepam^b (0.16 mg/kg, IV) and placed in right lateral recumbency. Subsequently, 0.25 mL of 2% lidocaine^c was injected ID in the skin superficial to the dorsal metatarsal artery. A 20-gauge, 1.5-inch, over-the-needle intra-arterial catheter^d was placed under aseptic conditions into the dorsal metatarsal artery, and a low-volume (0.9-mL) extension set^e was attached; the apparatus was secured with adhesive and protected with a bandage.

While the foal was still sedated, a polyethylene sampling line^f (outer diameter, 3 mm) was inserted through the left ventral meatus with the guidance of a preplaced nasotracheal tube^g (internal diameter, 8 mm); the sampling line was advanced into the trachea to a point just caudal to the thoracic inlet for measurement of Fio₂ and Petco₂. Placement of the tracheal catheter was confirmed radiographically. Additionally, a nasal cannula (internal diameter, 4 mm) that was made of soft plastic tubing^h was inserted into each ventral meatus so that the tip of each cannula was positioned in the nasopharynx at the level of the medial canthus of the eye. Each cannula was secured in place with tape and sutures.

Experimental protocol—Baseline values of rectal temperature, heart rate, and respiratory rate were recorded at least 1 hour after administration of the sedative, while each foal was standing. Immediately after collection of those baseline data, a baseline arterial blood sample (2 mL) was collected anaerobically into syringes containing heparin; syringes were immediately placed in an ice bath, and samples were analyzed within 10 minutes by use of a blood gas analyzer.ⁱ The blood gas analyzer was calibrated with reagent packs and gas standards prior to and every hour during each experimental procedure. Arterial blood samples were evaluated in duplicate; findings were corrected to rectal temperature, and the mean value for each variable was calculated.

Following collection of the baseline blood sample, each nasal cannula was connected to an individual air humidifier^j and flow meter^k and then connected to a flow splitter and a high-pressure tank that contained medical-grade (100%) oxygen. The tracheal catheter was interfaced with an airway gas analyzer^l that measured Fio₂ and Petco₂. The analyzer was calibrated prior to each procedure by use of gas supplied by the manufacturer. Each foal was observed for coughing, behavioral changes, or adverse effects during the approximately 3-hour experimental procedure period.

Each foal was manually restrained in a standing position in the stall with the mare present. Oxygen administration at the first predetermined rate was initiated, and a minimum of 5 minutes elapsed before measurements were made. A previous study³ in foals revealed that a 2-minute interval is adequate for equilibration. During the 5-minute equilibration period, the rate at which Fio₂ changed along with the fluctuations in Fio₂ was subjectively assessed until a stable reading was established. In 5 foals, oxygen was initially administered bilaterally (ie, through both nasal cannulae) and 4 rates of oxygen administration were evaluated. The flow rate for each cannula was initially 50 mL of oxygen/kg/min, which was adjusted to 100, 150, and 200 mL of oxygen/kg/min in sequence (total dosages of 100, 200, 300, and 400 mL of oxygen/kg/min, respectively). Those total dosages of supplemental oxygen corresponded to 6, 12, 18, and 24 L/min, respectively, in a 60-kg foal. In those 5 foals, oxygen was subsequently administered in the same sequence of increasing flow rates through only 1 randomly selected (ie, left or right) cannula (total dosages of 50, 100, 150, and 200 mL of oxygen/ kg/min). Those total dosages of supplemental oxygen corresponded to 3, 6, 9, and 12 L/min, respectively, in a 60-kg foal. In the other 4 foals, oxygen was initially administered bilaterally (ie, through both nasal cannulae) and the same 4 rates of oxygen administration were evaluated. However, the flow rate for each cannula was initially 200 mL of oxygen/kg/min, which was adjusted to 150, 100, and 50 mL of oxygen/kg/min in sequence (total dosages of 400, 300, 200, and 100 mL of oxygen/kg/min, respectively). In those 4 foals, oxygen was subsequently administered in the same sequence of decreasing flow rates through only 1 randomly selected (ie, left or right) cannula (total dosages of 200, 150, 100, and 50 mL of oxygen/kg/min). On the day that a foal was to be used in an experimental procedure, it was allocated to receive one or the other of the dosage regimens on an alternating schedule (ie, evaluated foals 1, 3, 5, 7, and 9 received the increasing flow rate regimen and evaluated foals 2, 4, 6, and 8 received the decreasing flow rate regimen).

For all foals, a minimum of 5 minutes was allowed to elapse before measurements were made at each flow rate; data collection at each flow rate was completed within 10 minutes. If a foal became excited during handling, it was allowed to regain a quiet demeanor with minimal restraint prior to collection of data. At each flow rate, measurements included assessments of rectal temperature, heart rate, and respiratory rate and the Fio₂ and Petco₂ values were obtained from a gas sample aspirated through the tracheal catheter; an arterial blood sample (2 mL) was collected and analyzed, as described. At the end of data collection at each oxygen flow rate, the foal was disconnected from all monitors and external devices and was allowed free access to the mare for at least 10 minutes. Prior to administration of oxygen at the various oxygen flow rates, the Fio₂ was evaluated to ensure that no residual effects from previous oxygen administration were present.

Statistical analysis—All data are reported as mean ± SD. A repeated-measures ANOVA was applied to each of the response variables (rectal temperature, heart rate, respiratory rate, Fio₂, pHa, Pao₂, Paco₂, Petco₂, blood bicarbonate concentration, TCO₂, Sao₂, and Pao₂:Fio₂ ratio) by use of computer software.^m For each response variable, an F test with Kenward and Roger adjustment to degrees of freedom was used to test for differences among the variable means of 9 data groups (baseline values and 8 treatment groups [bilateral administration of oxygen at rates of 50, 100, 150, or 200 mL/kg/min and unilateral administration of oxygen at rates of 50, 100, 150, and 200 mL/kg/min]) with significance set at a value of P < 0.05. When a significant F test was calculated, post hoc Tukey t tests were applied for pairwise comparisons between treatment means. To evaluate the effects of oxygen flow rate on 2 particular response variables, Fio₂ and Pao₂, a linear regression analysis with repeated measures was applied to each of the responses by use of computer software.^m The coefficient of determination also was calculated for the regression model for each response variable. In addition, the correlation coefficient between Paco₂ and Petco₂ was estimated and testedⁿ for significance. A value of P < 0.05 was considered significant.

Results

There were no complications associated with instrumentation or data collection in any foal. Most foals tolerated handling and restraint calmly, but some foals became excited; those foals were allowed to regain a quiet demeanor prior to collection of data. No adverse effects were observed during administration of oxygen at the lower flow rates (50, 100, and 150 mL/kg/min). However, foals developed signs of agitation during oxygen administration at the highest flow rate (200 mL/kg/min) exemplified by head tossing, rubbing of the muzzle, and hyperesthesia, regardless of whether oxygen was administered via 1 or both nasal cannulae. There were no significant differences among foals with regard to rectal temperature, heart rate, or respiratory rate at any oxygen flow rate, compared with baseline values (Table 1). Likewise, comparisons of data obtained at the various oxygen flow rates revealed no significant difference in rectal temperature, heart rate, or respiratory rate, with the exception of a significant (P = 0.04) difference in respiratory rate between unilateral administration of oxygen at a rate of 50 mL/kg/min and bilateral administration of oxygen at a rate of 100 mL/kg/min.

Data regarding Fio₂, pHa, Pao₂, Paco₂, Petco₂, blood bicarbonate concentration, TCO₂, Sao₂, and Pao₂: Fio₂ ratio were obtained for all foals at each oxygen flow rate (Table 2). The Fio₂ measurement fluctuated, depending on the foal's activity and respiratory rate, but generally increased and reached a plateau within 30 to 60 seconds of the commencement of oxygen administration at each flow rate. Compared with baseline values, significant (P < 0.001) increases in Fio₂, Pao₂, and Sao₂ were detected at all oxygen flow rates. Other significant differences from baseline values included changes in pHa during unilateral delivery of oxygen at a rate of 200 mL/kg/min (P = 0.04) and in Paco₂ during unilateral delivery at rates of 100 and 200 mL/kg/min and during bilateral delivery at a rate of 100 mL/kg/min (P < 0.04). Compared with baseline values, there were no significant differences in values of Petco₂, blood bicarbonate concentration, and TCO₂ at any oxygen flow rate, regardless of delivery method.

Administration of supplemental oxygen increased Fio₂ and Pao2 in a dose-dependent manner. However, at any given flow rate, measured variables were not affected by delivery method (ie, unilateral or bilateral administration). More specifically, values of the measured variables obtained during unilateral administration of 100 mL of oxygen/kg/min did not differ significantly from those obtained during bilateral administration of 50 mL of oxygen/kg/min; similarly, values of the measured variables obtained during unilateral administration of 200 mL of oxygen/kg/min did not differ significantly from those obtained during bilateral administration of 100 mL of oxygen/kg/min.

In addition, comparisons among individual oxygen flow rates delivered by either method revealed significant (P ≤ 0.02) differences in Fio₂, with the exception of 100 mL/kg/min administered bilaterally versus 150 mL/kg/min administered unilaterally, 150 mL/kg/min administered bilaterally versus 200 mL/kg/min administered unilaterally, and 150 mL/kg/min administered unilaterally versus 200 mL/kg/min administered unilaterally. Also, comparisons among individual oxygen flow rates delivered by either method revealed significant (P ≤ 0.03) differences in Pao₂, with the exception of 100 mL/kg/min administered bilaterally versus 150 mL/kg/min administered bilaterally, 100 mL/kg/min administered bilaterally versus 150 mL/kg/min administered unilaterally, 150 mL/kg/min administered bilaterally versus 200 mL/kg/min administered unilaterally, and 150 mL/kg/min administered unilaterally versus 200 mL/kg/min administered unilaterally. With regard to the Pao₂:Fio₂ ratio, a significant difference between 200 mL of oxygen/kg/min administered bilaterally and 50 mL of oxygen/kg/min administered unilaterally (P = 0.03) and between 50 mL of oxygen/kg/min administered unilaterally and 150 mL of oxygen/kg/min administered unilaterally (P = 0.04) was detected. No significant differences in pHa, Paco₂, Petco₂, blood bicarbonate concentration, and TCO₂ were identified among individual oxygen flow rates.

Linear regression analysis yielded equations for Fio₂ and Pao₂ associated with unilateral or bilateral oxygen delivery (Table 3). The coefficient of determination was 0.9223 for the regression model of Fio₂ and 0.8632 for the regression model of Pao₂. In other words, the linear regression model could explain 92.23% and 86.32% of the variation in Fio₂ and Pao₂, respectively. There was a significant correlation (r = 0.497; P < 0.001) between Paco₂ and Petco₂.

Discussion

Results of the study reported here indicated that Pao₂ and Fio₂ increased in a dose-dependent manner as the flow of supplemental oxygen into the nasopharynx of healthy neonatal foals increased. Intuitively, this was an expected response to oxygen administration. Nevertheless, these findings support the rationale for nasopharyngeal administration of supplemental oxygen in hypoxemic foals and provide a dosage guide for oxygen administration as well as expected changes in Pao₂ and Fio₂ in response to treatment with oxygen in healthy neonatal foals. Also, data obtained in the present study indicated that measured variables did not differ when oxygen was administered at a specific flow rate through 1 or 2 nasal cannulae; this suggests that oxygen administration via 1 nasal cannula can provide adequate changes in Fio₂ and Pao₂, within certain flow rate limits. If a maximum increase in Fio₂ in healthy neonatal foals is desired, nasopharyngeal administration of oxygen at a rate of 200 mL/kg/min simultaneously in each naris (400 mL/kg/min total) can increase the Fio₂ to approximately 75%.

Physiologically, nasopharyngeal administration of oxygen increases the Fio₂, thereby allowing higher concentrations of oxygen to reach the alveoli; consequently, this creates a higher concentration gradient of oxygen between the alveoli and arterial blood within the pulmonary vasculature. The increase in Fio₂ is a result of direct flow of supplemental oxygen into the trachea and the capacity of the nasopharynx to act as a reservoir for inspired air (ie, oxygen).¹² During supplemental oxygen administration, the nasopharynx is progressively filled with higher concentrations of oxygen, particularly during the pause in air movement between expiration and inspiration. The fixed volume of air contained within the nasopharynx is gradually filled with supraphysiologic concentrations of oxygen, thereby increasing the Fio₂ upon inspiration.¹² The pause between expiration and inspiration will vary with the respiratory rate; therefore, higher oxygen flow rates may be necessary to achieve anticipated Fio₂ values in animals with higher respiratory rates.¹⁸ This is supported by the fact that Fio₂ is inversely related to respiratory rate in infants receiving oxygen via intranasal administration.^18,19 Other factors that affect the Fio₂ in infants and foals include cannula flow rate, the Fio₂ in the cannula gas flow, patency of cannula openings, placement of the nasal cannula, patient's body weight, minute ventilation, and the relative duration of inspiration and expiration.^1,19

On the basis of the present study's results, it is apparent that there is a rapid change in Fio₂ and Pao₂ in response to administration of supplemental oxygen in healthy neonatal foals. Increases in Fio₂ were observed within 30 to 60 seconds after commencement of oxygen administration, similar to findings in other species.¹² In addition, based on the rapid decrease in Fio₂ once supplemental oxygen administration was discontinued, clearance of oxygen was rapid—a factor that should be considered when administering supplemental oxygen in a clinical setting. Another point of interest was the irritation or discomfort caused by unilateral or bilateral intranasal administration of oxygen at a flow rate of 200 mL/kg/min in the foals in the present study. However, the authors have administered supplemental oxygen at flow rates > 200 mL/kg/min to ill neonatal foals without observing adverse effects. It is likely that ill neonatal foals are lethargic and less responsive to the irritation caused by high rates of oxygen administration. Nonetheless, if nasal irritation or discomfort develops during unilateral administration of oxygen at a specific flow rate, distribution of the same total flow rate through 2 nasal cannulae may be a viable alternative delivery method. Despite the high flow rates of oxygen, no retardation of exhalation or trapping of carbon dioxide was evident in the foals of the present study. Although there was a significant increase in Paco₂ during unilateral administration of oxygen at flow rates of 100 and 200 mL/kg/min and during bilateral administration at a flow rate of 200 mL/kg/min, compared with baseline values, the degree of hypercapnea was considered clinically unimportant in the healthy study foals. Moreover, no significant differences were detected between baseline Petco₂ and Petco₂ values at the individual oxygen flow rates. However, in infant studies,^20,21 the administration of oxygen via nasal cannula generated positive end-expiratory pressure, depending on the size of the nasal cannula (with respect to infant size) and flow rate. Therefore, it is possible that positive end-expiratory pressure can be generated in neonatal foals receiving supplemental oxygen via nasal cannula, particularly in ill foals that have decreased or weakened respiratory effort as a result of exhaustion or weak contraction of respiratory muscles.¹ This can potentially result in elevated airway pressure with both positive (increased functional residual capacity, alveolar recruitment, and improvement in ventilation-perfusion matching) and negative (retention of carbon dioxide and hypercapnia) consequences, especially at high oxygen flow rates.^1,21

The relationship and correlation between Paco₂ and Petco₂ has been examined in various studies^22–24 in efforts to use Petco₂ as a less invasive means of monitoring Paco₂ in clinical cases such as emergency room admissions and during anesthesia; overall correlation between these 2 variables has been high in several studies^22–24 in people. Likewise, a significant correlation between Paco₂ and Petco₂ was determined in the healthy neonatal foals used in the present study. However, the actual correlation between Petco₂ and Paco₂ was only moderate (r = 0.497). This can be partially explained by the fact that administration of supplemental oxygen had a significant effect on Paco₂ but not on Petco₂. Therefore, oxygen administration accounted for part of the variation in Paco₂ that was not correlated with Petco₂. Nevertheless, it is possible that Petco₂ could be used to reflect and monitor changes in Paco₂ in ill foals, although further studies are necessary. It should be noted that the gas sample used for measurement of Petco₂ in the present study was aspirated from the intrathoracic portion of the trachea rather than from the nares or nasopharynx, which are more easily accessible locations and are more likely to be used for Petco₂ measurement in ill foals. The possibility that the anatomic location at which Petco₂ is measured may change Petco₂ values slightly requires further investigation.

One important reason to attempt to estimate Fio₂ is the ability to use the Pao₂:Fio₂ ratio to evaluate pulmonary gas exchange in hypoxemic patients and to assess respiratory tract disease severity. Acute lung injury is defined as a Pao₂:Fio₂ ratio < 300 mm Hg (but > 200 mm Hg), whereas ARDS is defined as a Pao₂:Fio₂ ratio < 200 mm Hg (along with other previously described criteria).^14–16 Specific modifications to the definition of ALI and ARDS have been made to account for the documented changes in gas exchange efficiency that develop in neonatal foals (< 7 days old) as well as in infants.^15,25 In the consensus definitions of ALI and ARDS in veterinary medicine, the threshold of equine neonatal ALI is defined as a Pao₂:Fio₂ ratio of < 250 mm Hg, whereas equine neonatal ARDS is defined as a Pao₂:Fio₂ ratio of < 160 mm Hg at 4 days after birth.¹⁵ The Pao₂:Fio₂ ratio that was considered normal in that report¹⁵ was a value > 400 mm Hg. In the study reported here, the mean Pao₂:Fio₂ ratio in healthy neonatal foals (mean age, 3.9 days) ranged from 501 to 594 mm Hg and was established in standing foals that were, at times, receiving intranasal administration of supplemental oxygen. The difference in the Pao₂:Fio₂ ratio between the present and previous studies^15,26,27 may be explained, in part, by the fact that the consensus definitions were based on arterial blood gas values from foals that were breathing room air in lateral recumbency, a position that is known to decrease Pao₂ values. Overall, only a few veterinary reports^13,14 have documented the use of the Pao₂:Fio₂ ratio in foals, and accordingly, the use of the Pao₂:Fio₂ ratio in neonatal foals with pulmonary diseases is in its infancy. The information obtained from the study of this report confirmed that the mean Pao₂:Fio₂ ratio in healthy neonatal foals that are breathing room air should be approximately 500 mm Hg (range, 477 to 594 mm Hg). Furthermore, this information can be used to estimate the Fio₂ in hypoxemic neonatal foals, which will facilitate the further investigation of the Pao₂:Fio₂ ratio in clinical cases. Clearly, additional studies are necessary to assess Pao₂:Fio₂ ratio values in foals with ALI or ARDS and evaluate the sensitivity and specificity of the extrapolated threshold ratios for diagnosis of ALI and ARDS in neonatal foals.

Another reason to be aware of the Fio₂ induced by administration of supplemental oxygen in neonatal foals is to avoid development of oxygen toxicosis as a result of high flow rates of oxygen. On the basis of the findings of the present study, it is unlikely that the recommended maximum Fio₂ (60%) during supplemental oxygen administration or mechanical ventilation^11,12 would be exceeded, particularly with unilateral administration of the oxygen dosages investigated. However, in severely hypoxemic neonatal foals, bilateral nasal cannulae have been used to administer oxygen in combined flow rates of up to 30 L/min (eg, administration of 250 mL of oxygen/kg/min in each naris in a 60-kg foal).¹ The maximum mean Fio₂ measured in the present study was approximately 75% when foals received oxygen intranasally at a rate of 200 mL/kg/min bilaterally. Maintenance of a unilateral oxygen flow rate of ≤ 200 mL/kg/min or a bilateral flow rate of ≤ 150 mL/ kg/min should avoid excessively high Fio₂ concentrations in neonatal foals, if prolonged intranasal administration of oxygen is necessary. The guidelines set forth by the Society of Critical Care Medicine recommend that the lowest possible Fio₂ should be used at all times to achieve treatment goals and should not exceed 50% in patients with respiratory failure.²⁸

Although it is important to be cognizant of the Fio₂ to avoid development of oxygen toxicosis and to evaluate the efficacy of pulmonary gas exchange, the clinical endpoints of supplemental oxygen administration are improved Pao₂ and Sao₂. The value of Pao₂ in foals receiving unilateral administration of oxygen intranasally at a flow rate of 200 mL/kg/min in the present study (mean Pao₂, 269.7 mm Hg) was similar to the finding in slightly younger foals receiving unilateral administration of oxygen intranasally at a flow rate of 10 L/min in another study³ (mean Pao₂, 268.5 mm Hg). At the flow rates used in the present study, the mean maximum Pao₂ values that could be achieved via unilateral and bilateral intranasal oxygen administration in healthy neonatal foals are approximately 270 and 375 mm Hg, respectively. However, this information is of limited clinical use in ill neonatal foals with compromised cardiopulmonary function (ie, diffusion impairment, ventilation-perfusion mismatch, or intrapulmonary or intracardiac right-to-left shunting of blood) that results in impaired alveolar gas exchange and hypoxemia.²⁹ For example, in 1 study,³⁰ the mean Pao₂ value in response to administration of supplemental oxygen via facemask was significantly decreased in abnormal neonatal foals, compared with the value in similarly treated healthy neonatal foals (mean Pao₂, 129.4 and 312.8 mm Hg, respectively). Therefore, adjustment of the flow rate of supplemental oxygen in ill foals with cardiopulmonary disease should be based on evaluation of the response to supplemental oxygen administration (eg, measurement of Pao₂ and Sao₂). Physiologically, as Pao₂ increases, Sao₂ concomitantly increases. Not surprisingly, Sao₂ increased from baseline (as Pao₂ increased) during oxygen administration at all of the flow rates used in the present study. Recommended therapeutic goals of oxygen administration in neonatal foals include maintenance of Pao₂ at 80 to 110 mm Hg and Sao₂ > 90%.^1,28

In the study reported here, other significant differences in measured variables were detected when findings at the individual oxygen flow rates were compared with baseline values or with one another. Compared with the baseline value, there was a significant decrease in pHa during unilateral administration of oxygen at a rate of 200 mL/kg/min, but the difference between the 2 values (0.024) is not likely to have any clinical importance. Furthermore, the exact reason why respiratory rate during unilateral administration of 100 mL of oxygen/kg/min and during bilateral administration of 100 mL of oxygen/kg/min differed significantly is unknown. Although restraint of the foals could have resulted in excitement, no specific explanation could be provided for this observation.

One distinct limitation of the present study that should be highlighted was the varied temperaments of the foals. Most foals tolerated handling and restraint without resentment. However, some foals became very excited upon handling, which increased heart and respiratory rates and potentially altered the variables being measured. In particular, Fio₂ appeared to fluctuate the most, depending on the foal's activity and respiratory rate. If a foal was excited, the investigators allowed the foal to regain a quiet demeanor with minimal restraint prior to collection of data. Nonetheless, the few highly anxious foals may have provided skewed results. Another limitation of the study was that the foals were all in good health, and the response to nasopharyngeal administration of supplemental oxygen may be different in ill neonatal foals with pulmonary disease. Evaluation of the response to nasopharyngeal administration of oxygen at different flow rates in ill neonatal foals, including those with pulmonary diseases, is warranted.

Results of the present study have indicated that nasopharyngeal administration of supplemental oxygen effectively increases Fio₂, Pao₂, and Sao₂ and allows clinicians to estimate Fio₂ in neonatal foals. Previously recommended oxygen flow rates in foals vary from 2 to 15 L/min, depending on the size, needs, and response of the foal.^1,31,32 Information obtained from the present study has provided linear regression equations to estimate the Fio₂ (based on body weight) in neonatal foals in response to different oxygen flow rates and to predict the response (ie, Pao₂) to a specific oxygen flow rate in healthy neonatal foals and subsequently compare this theoretical response with the response of an ill foal. It should be emphasized that the findings of the present study and the linear regression equations are estimates of Fio₂ and Pao₂ in response to nasopharyngeal administration of supplemental oxygen in healthy standing neonatal foals and should not be used as absolute therapeutic values or goals. Adequate response to oxygen administration is best evaluated by monitoring arterial blood gas variables such as Pao₂ and Sao₂ and the clinical response of the patient.