Materials and Methods

Animals—This prospective study included all neonatal foals (≤ 10 days of age) admitted to or born at the Lloyd Veterinary Medical Center at Iowa State University between January and May 2010, in which an arterial blood gas analysis was performed as part of their diagnostic evaluation. This included healthy foals born from mares admitted for monitoring and facilitation of parturition, healthy and ill foals born from mares with placentitis, and ill foals admitted for various medical disorders. Foals were considered healthy on the basis of physical examination, adequate transfer of maternal antibodies, and historical absence of maternal disorders during gestation or parturition. Definitive diagnosis in ill foals was based on clinical and diagnostic evaluation, which may have included a CBC, serum biochemical analysis, aerobic and anaerobic bacterial culture of blood samples, evaluation of serum immunoglobulin concentration, and ancillary diagnostic tests such as radiography and ultrasonography. Not all diagnostic testing was performed on all ill foals but was left to the discretion of the attending clinician. The experimental protocol was approved by the Institutional Animal Care and Use Committee of Iowa State University.

Procedures—Arterial blood samples were collected anaerobically into heparinized syringes from the dorsal metatarsal artery in all foals while in lateral recumbency at different times throughout hospitalization. All samples were analyzed within 5 minutes by use of a blood gas analyzer^a; blood gas measurements (Paco₂ and Pao₂) were corrected to the foal's rectal temperature but not for the elevation at which the experiment was conducted (280.4 m [920 feet]). The Sao₂ was obtained from measured Pao₂ by use of a dissociation curve described for equine hemoglobin.¹⁴ The blood gas analyzer was calibrated with reagent packs and gas standards prior to and every hour of each day during experimentation. Within 2 minutes after collection of arterial blood, and while foals were still in lateral recumbency, a reflectance transducer^b was positioned over the coccygeal artery until a strong and consistent signal was detected, then was secured to the tail base with adhesive tape for indirect measurement of Spo₂ by use of a commercial patient monitor.^c Consecutive measurements of Spo₂ data were continuously recorded over a 2-minute period. Values of Spo₂ were recorded only if the pulse rate displayed on the oximeter was equal to the heart rate indicated by thoracic auscultation. Additionally, to obtain a sample of gas from the nasopharynx, a modified nasal tube (endotracheal tube with a 7-mm outer diameter cut to 4 cm in length) was connected to a side-stream capnograph and then inserted deep into a naris of the foal. Consecutive measurements of respiratory rate and Petco₂ were continuously monitored and recorded for 2 minutes by use of a commercially available capnograph.^c The capnograph was calibrated prior to experimental use by means of manufacturer-supplied gas. The Spo₂ and Petco₂ values were subsequently averaged with the mean value used for subsequent analysis.

Statistical analysis—Sample mean ± SD values were calculated for all variables. The association between Petco₂ and Paco₂ was assessed by use of Pearson correlation coefficients and tested for significance. Similarly, the association between Spo₂ and Sao₂ was assessed by use of Pearson correlation coefficients and tested for significance.

To assess levels of agreement, differences were calculated and summarized by use of mean ± SD values between the paired values of Petco₂ and Paco₂ and between the paired values of Sao₂ and Spo₂. The 95% limits of agreement were calculated as mean difference ± 2 SD of the difference.¹⁵ A paired t test was applied to test the difference of the mean value for each of the pairs. The association between paired differences and the variables respiratory rate, heart rate, and rectal temperature was assessed by use of Pearson correlation coefficients. The association between paired differences and health status (healthy or ill) was assessed by use of a 2-sample t test. Values of P ≤ 0.05 were considered significant. Correlation coefficients were interpreted as weak (< 0.4), moderate (0.4 to 0.7), or strong (> 0.7).⁵

Results

Thirty-one neonatal foals were evaluated during the study period; breeds included Quarter Horse (n = 13), Thoroughbred (9), Paint (6), Percheron (1), Appaloosa (1), and Standardbred (1). Foals had a mean age of 4.1 days (range, 1 to 10 days) and a mean body weight of 52.7 kg (115.9 lb; range, 38 to 68 kg [83.6 to 149.6 lb]). Various coat colors were represented including bay and sorrel. There were 13 fillies and 18 colts, of which 10 were healthy and 21 were ill. Medical disorders of ill foals included failure of passive transfer of maternal antibodies, septicemia, enteritis and colitis, neonatal encephalopathy, patent urachus, neonatal isoerythrolysis, musculoskeletal disorders, congenital aganglionosis, and intussusception; some ill foals had > 1 concurrent disorder. The mean ± SD rectal temperature, heart rate, and respiratory rate were 38.2 ± 0.6°C (100.7 ± 1.0°F), 99 ± 19.8 beats/min, and 36 ± 18 breaths/min, respectively.

Regarding CO₂ values, the mean ± SD measurements of Paco₂ and Petco₂ for healthy foals were 49.2 ± 3.7 mm Hg and 48.5 ± 6.0 mm Hg, respectively, whereas mean measurements for ill foals were 48.3 ± 9.1 mm Hg and 48.5 ± 8.6 mm Hg, respectively. There was no significant difference in the mean values of Paco₂ or Petco₂ between the 2 groups; therefore, all individual measurements from healthy and ill foals were pooled, yielding a mean ± SD Paco₂ and Petco₂ of 48.6 ± 7.8 mm Hg (range, 42.8 to 67.1 mm Hg) and 48.5 ± 7.7 mm Hg (range, 33.4 to 66.3 mm Hg), respectively. There was a strong and significant linear correlation (r = 0.792; P < 0.001) between Paco₂ and Petco₂ with the calculated 95% limits of agreement of −9.9 to 10.1 mm Hg (Figures 1 and 2). The mean ± SD Paco₂–Petco₂ gradient was 0.7 ± 4.4 mm Hg for healthy foals and −0.2 ± 5.3 mm Hg for ill foals, with no significant difference between the means; therefore, the values of healthy and ill foals were pooled, yielding a mean ± SD Paco₂–Petco₂ gradient of 0.1 ± 5.0 mm Hg. Individual Petco₂ measurements were within ± 2 mm Hg of Paco₂ in 13 of 31 foals, within ± 5 mm Hg of Paco₂ in 24 of 31 foals, and within ± 10 mm Hg of Paco₂ in 26 of 31 foals. There was no significant correlation between the mean Paco₂–Petco₂ gradient and respiratory rate, heart rate, or rectal temperature. As noted, the difference between the mean ± SD Paco₂ and Petco₂ in all foals (ie, the Paco₂–Petco₂ gradient) was 0.1 mm Hg.

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Scatterplot of paired measurements of Petco₂ and Paco₂ for 31 conscious neonatal foals (10 healthy and 21 ill). The solid line represents the line of identity.

Citation: Journal of the American Veterinary Medical Association 239, 10; 10.2460/javma.239.10.1341

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Bland-Altman plot of the difference between Paco₂ and Petco₂ versus the mean of Paco₂ and Petco₂. Paired measurements of Paco₂ and Petco₂ were used to determine the partial pressure of CO₂ in 31 conscious neonatal foals (10 healthy and 21 ill). Dashed horizontal lines represent the 95% limits of agreement (ie, mean difference ± 2 SD).

Citation: Journal of the American Veterinary Medical Association 239, 10; 10.2460/javma.239.10.1341

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The reflectance transducer, placed at the base of the tail, provided a reliable pulse rate comparable with that obtained via thoracic auscultation in all foals. The mean ± SD Sao₂ and Spo₂ for healthy foals were 96.2 ± 1.4% and 93.2 ± 3.5%, respectively, whereas mean measurements for ill foals were 95.3 ± 2.5% and 93.1 ± 4.1%, respectively. There was no significant difference in the mean values of Sao₂ or Spo₂ between healthy and ill foals; therefore, individual measurements from healthy and ill foals were pooled, yielding a mean ± SD Sao₂ and Spo₂ of 95.6 ± 2.2% (range, 88.9% to 97.8%) and 93.1 ± 3.9% (range, 85.3% to 100.0%), respectively. The mean value of Sao₂ was significantly (P < 0.001) higher than that of Spo₂. There was a moderate and significant linear correlation (r = 0.450; P = 0.011) between Sao₂ and Spo₂ (Figure 3). Calculated 95% limits of agreement were −4.5% to 9.5% (Figure 4). The mean ± SD difference between reported Sao₂ and Spo₂ was 3.0 ± 3.4% for healthy foals and 2.3 ± 3.6% for ill foals, with no significant difference between the means; therefore, the values of healthy and ill foals were pooled, yielding a mean ± SD difference between Sao₂ and Spo₂ of 2.5 ± 3.5%. Individual Sao₂ values were within ± 2% of Spo₂ values in 10 of 31 foals, within ± 5% in 22 of 31 foals, and within ± 10% in 31 of 31 foals. In addition, there was no significant correlation between the mean Sao₂ and Spo₂ difference and respiratory rate, heart rate, or rectal temperature.

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Scatterplot of paired measurements of Spo₂ and Sao₂ for 31 conscious neonatal foals (10 healthy and 21 ill). The solid line represents the line of identity.

Citation: Journal of the American Veterinary Medical Association 239, 10; 10.2460/javma.239.10.1341

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Bland-Altman plot of the difference between Sao₂ and Spo₂ versus the mean of Sao₂ and Spo₂. Paired measurements of Sao₂ and Spo₂ were used to determine the saturation of hemoglobin with oxygen in 31 conscious neonatal foals (10 healthy and 21 ill). Dashed horizontal lines represent the 95% limits of agreement (ie, mean difference ± 2 SD).

Citation: Journal of the American Veterinary Medical Association 239, 10; 10.2460/javma.239.10.1341

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Discussion

Both hypercapnia and hypocapnia can be detrimental to neonatal foals. Hypercapnia results in respiratory acidemia and cerebral vasodilation, which can subsequently increase cerebral blood flow and intracranial pressure; these changes can consequently result in intracranial hemorrhage.^16,17 Conversely, hypocapnia can increase the risk for cerebral injury as a result of decreased blood flow to the brain, leading to ischemia of the white matter.^16,17 Thus, maintaining the Paco₂ concentration within the range observed in healthy individuals is an important goal in the care of critical patients. One particular situation in which foals can become substantially hypercapnic is with the clinical syndrome of neonatal encephalopathy.^18,19 A noninvasive method of estimating Paco₂ and detecting hypercapnia or hypocapnia would improve clinical evaluation and monitoring of ill foals with underlying ventilatory or pulmonary disorders and would guide treatment while avoiding frequent arteriopuncture. Results of this study support the use of Petco₂ monitoring as an estimate of Paco₂ in ill neonatal foals on the basis of a significant and strong correlation and relatively good agreement between the 2 measurements.

Although Petco₂ was strongly correlated with Paco₂ in this study (r = 0.792), correlation is a measure of association between 2 measurements, rather than agreement between 2 measurements. Perfect correlation exists between 2 methods when pairs of measurements approximate a straight line. However, interpretation of correlation can be deceiving; for example, if 2 different rectal thermometers always differ by 10°C (50°F), the 2 thermometers are strongly correlated but their level of agreement is low. Perfect agreement exists between 2 methods when pairs of measurements lie along a line of unity with a slope of 1 and an intercept of 0.¹⁵ Therefore, it is agreement, rather than correlation, that determines whether one method of measurement can replace another.²⁰ The 95% limits of agreement between Paco₂ and Petco₂ in this study were −9.9 to 10.1 mm Hg, indicating that 95% of Petco₂ measurements were from 10.1 mm Hg less than to 9.9 mm Hg greater than measured Paco₂. This range can be subjectively interpreted in different ways. In an analogous study⁵ evaluating the agreement between Paco₂ and Petco₂ in dogs, the 95% limits of agreement (−5.7 to 14.1 mm Hg) were similar to those documented in the study presented here.⁵ The authors of the aforementioned study in dogs concluded that Petco₂ was a clinically useful method of monitoring ventilation in ill dogs. Conversely, the 95% limits of agreement in a comparable study⁶ in children were −12.9 to 5.5 mm Hg; in that study, the authors concluded that this range was clinically too imprecise to replace Paco₂. In the present study, we consider the 95% limits of agreement between Petco₂ and Paco₂ as an acceptable adjunctive method of estimating and monitoring changes in Paco₂, especially considering that 77.4% of Petco₂ measurements were within 5 mm Hg of paired Paco₂ measurements. Additionally, the limits of agreement in the present study (10.1 mm Hg) were better than those in the aforementioned studies in dogs (14.07 mm Hg)⁵ and children (12.88 mm Hg),⁶ as the present study was smaller in magnitude than those previous studies. Moreover, the mean Paco₂–Petco₂ gradient was only 0.1 mm Hg, indicating little bias in the use of Petco₂ to approximate Paco₂. Together, this information suggests that Petco₂ can be used to estimate Paco₂ and monitor ventilatory status in conscious, spontaneously breathing neonatal foals. In the present study, there was no correlation between the mean Paco₂–Petco₂ gradient nor mean difference between Sao₂ and Spo₂ and respiratory rate, heart rate, or rectal temperature, suggesting that variations in these variables such as tachypnea, tachycardia, or fever, which are commonly observed in ill foals, do not significantly alter the association between direct and indirect measured values of Paco₂ or Sao₂. As with any indirect clinicopathologic measurements, periodic direct measurement of Paco₂ is a prudent approach to monitor patients, especially when drastic changes are observed in indirect measurements.

Previous studies^3,21–23 have evaluated the use of capnography (Petco₂) to monitor Paco₂ in anesthetized adult horses and foals. In 1 study²² involving anesthetized adult horses, there was a significant correlation (r = 0.805; P < 0.001) between Petco₂ and Paco₂, with a mean ± SD Paco₂–Petco₂ gradient of 11.9 ± 8.1 mm Hg for halothane anesthesia. Those authors concluded that Petco₂ monitoring was an acceptable means of monitoring respiratory acid-base balance. Alternatively, authors of another study²³ did not recommend capnography as a method of evaluating Paco₂ on the basis of poor limits of agreement between Petco₂ and Paco₂ (−20.1 to 8.7 mm Hg) in anesthetized adult horses. In a study³ involving anesthetized foals, the mean ± SD Paco₂–Petco₂ gradient was 7 ± 5 mm Hg (5 to 60 minutes after induction). This difference significantly increased to 13 ± 5 mm Hg 65 to 90 minutes after induction. The authors concluded that Petco₂ was useful in predicting changes in Paco₂ during the early (< 60 minutes) anesthetic period, but also stated that the margin for error in predicting Paco₂ from Petco₂ was unacceptable for making clinical judgments about ventilatory status in anesthetized foals.³ In previous equine studies^3,22,23 comparing Paco₂ and Petco₂, it is clear that anesthesia negatively impacts the association between these variables because of the effects of general anesthesia and prolonged recumbency resulting in hypoventilation, increased respiratory dead space, and ventilation-perfusion mismatch.^3,22,23 Although the difference between Paco₂ and Petco₂ in the study reported here was much less than that reported for anesthetized animals, direct comparisons between studies are not possible, as the population of our study consisted of conscious foals.

There was no significant difference in the Paco₂–Petco₂ gradient between healthy and ill foals in the present study; thus, values obtained from both healthy and ill neonatal foals were combined, resulting in the reported Paco₂–Petco₂ gradient of 0.1 ± 5.0 mm Hg. A number of equine studies have also evaluated the Paco₂–Petco₂ gradient in anesthetized horses and foals, but to the authors' knowledge, this is the first evaluation of the Paco₂–Petco₂ gradient in conscious foals. As noted in the previous study³ on foals, the mean Paco₂–Petco₂ gradients were 7 and 13 mm Hg at 5 to 60 minutes and 65 to 90 minutes, respectively, after anesthetic induction.³ Other studies^3,4,21,22 in anesthetized adult horses also reflect a higher Paco₂–Petco₂ gradient in anesthetized horses, and this fact has been attributed to increased physiologic dead space, increased ventilation-perfusion ratio, and hypoventilation, among other factors.^3,4,21,22 Clinically, the Paco₂–Petco₂ gradient can be used to document and monitor a variety of respiratory or cardiac conditions.^24–28 For example, neonatal infants with pulmonary disorders such as persistent pulmonary hypertension, respiratory distress syndrome, pneumonia, or meconium aspiration had a significantly higher Paco₂–Petco₂ gradient (7.4 ± 3.3 mm Hg) when compared with aged-matched healthy controls (3.0 ± 2.4 mm Hg).²⁵ The Paco₂–Petco₂ gradient has also been used to support the diagnosis of pulmonary thromboembolism as well as to monitor efficacy of thrombolysis in patients with pulmonary thromboembolism.^27,28 Therefore, the Paco₂–Petco₂ gradient can be used to evaluate or monitor progression of various pulmonary or cardiovascular diseases.

In the study reported here, there were instances in which the Petco₂ was higher than the Paco₂ (Figures 1 and 2). In theory, this should not occur, but this finding has been reported in similar studies^{5,6,9,23,29,30} on people, horses, and dogs. This detail may have contributed to the small Paco₂–Petco₂ gradient documented in our study. The exact reason for the occurrence in the present study is unknown, but possible reasons include the temporal delay between collection and measurement of Paco₂ and measurement of Petco₂, errors in calibration of the capnograph or blood gas analyzer, overestimation of Petco₂ from interference of water vapor in the capnograph's sampling chamber, or trapping of CO₂ within the nasopharynx because of increased expiratory resistance from nasopharyngeal obstruction or presence of the measuring chamber.³¹ The fact that Paco₂ was measured at a single time point whereas the Petco₂ was the mean measurement obtained over 2 minutes may have also impacted results. Other proposed causes of a higher Petco₂, compared with Paco₂, include excessive CO₂ production coupled with low inspired volume or high cardiac output, CO₂ displacement from hemoglobin as a result of high inspired O₂ content, low functional residual capacity, and alveoli with low ventilation-to-perfusion ratios.^32,33

Just as hypercapnia or hypocapnia can be detrimental to the health of foals, hypoxemia can be equally harmful. Pulse oximetry is a monitoring technique that provides immediate information about the patient's pulse rate and oxygenation status and has been investigated in anesthetized horses and foals.^{13,23,34–37} A previous study¹³ in neonatal foals documented a significant and strong correlation between Sao₂ and Spo₂ (r = 0.93; P < 0.001) with a reflectance probe in anesthetized foals; in that study, Spo₂ underestimated Sao₂, with a mean difference between Sao₂ and Spo₂ of 5.3%.¹³ Results of the present study are the first to report comparisons between Sao₂ and Spo₂ in conscious neonatal foals and suggest that Spo₂ measured with a reflectance probe^c placed at the base of the tail is a feasible method of monitoring Sao₂.

In the present study, Spo₂ tended to underestimate Sao₂, with a mean difference of 2.5%. Interestingly, other studies^13,23,36,37 on horses have also documented that Spo₂ generally underestimates Sao₂. In the study reported here, the limits of agreement were −4.5% to 9.5%, indicating that 95% of Spo₂ measurements were from 9.5% less than to 4.5% greater than Sao₂. Manufacturers report pulse oximetry accuracy to 1 SD of < ± 3% when arterial oxygen saturation is ≥ 70%.¹² To incorporate the 95% confidence interval, this number is doubled (eg, < ± 6%). Thus, the manufacturer's reported accuracy is open to interpretation. Overall, pulse oximetry appears to provide a good estimate of Sao₂ and allows clinicians to monitor changes in pulse and hemoglobin saturation in conscious neonatal foals. Even though 71% of Spo₂ values were within 5% of Sao₂, the authors believe that the limits of agreement in the study reported here are large enough to indicate that Spo₂ cannot supplant precise determination of Sao₂ via arterial blood gas analysis. Additionally, although the correlation between Sao₂ and Spo₂ in the present study was significant, the actual correlation (r = 0.499) was moderate at best. Therefore, arterial blood gas analysis should be used to confirm and monitor Spo₂ changes (ie, desaturation of hemoglobin).

Transmittance probes use a phototransmitter on one side of a tissue bed while the photodetector is on the other side of the tissue bed, thus requiring a thin extremity (eg, ear or finger) or body structure (eg, lip or tongue) to be isolated or clamped between the phototransmitter and photodetector. A reflectance probe, in which both the phototransmitter and photodetector are on the same side of the tissue bed, was selected for the present study because, in the authors' clinical experience, transmittance probes have an inconsistent ability to detect a pulse in foals. This observation is supported by equine studies^34,36 that failed to detect the pulse with transmittance probes placed on a nostril, a lip, or the vulva. Furthermore, some transmittance probes do not work consistently on darkly pigmented tissue.^34,36 Of note, consistent detection of the pulse has been documented when the transmittance probe is placed on the tongue^{13,23,34,36,37}; however, this site is not particularly feasible in conscious foals. In the study reported here, the reflectance probe was always able to detect the foal's pulse and provide an Spo₂ reading, regardless of skin pigmentation. Considering the ease of placement and maintenance of the reflectance probe in proper position on the ventral aspect of the tail base, the ability to consistently detect a pulse, and the relatively good agreement with Sao₂ measurements, the authors suggest that placement of a reflectance probe at this site is an ideal method of monitoring pulse rate and Sao₂ in foals, particularly if the foal is recumbent for prolonged periods because of illness. In turn, real-time and continuous assessment of the pulse and Spo₂ on a moment-to-moment basis will facilitate patient monitoring as well as response to therapeutic interventions. However, the authors would like to reiterate that Spo₂ cannot completely supplant arterial blood gas analysis on the basis of the findings in the present study.

There are several limitations of this study that should be considered. First, simultaneous determination of measurements, such as Paco₂ and Petco₂, was not possible; therefore, the gap in time (2 to 5 minutes) between measurements could have resulted in temporal differences between direct and indirect measurements. Another limitation is the fact that clinical patients were studied; therefore, deliberate hypercapnia or hypocapnia and hypoxemia could not be induced. The Paco₂ in this study ranged from 42.8 to 67.1 mm Hg; thus, correlations between extremely low or high Paco₂ values and Petco₂ were not investigated. Similarly, Sao₂ in this study ranged from 88.9% to 97.8%; thus, correlation between Sao₂ and Spo₂ cannot be made with lower (eg, < 80%) Sao₂ values. A prior study¹³ in which foals were anesthetized allowed manipulation of the Pao₂ and Sao₂. In that study,¹³ the authors concluded that poor precision of Spo₂ occurred when Sao₂ values were < 80%. However, the authors also stated that the reflectance probe performed more consistently over various ranges of Sao₂ than did other transmittance probes.¹³ Other studies^36,37 in anesthetized adult horses have also documented increased variability in the difference between Sao₂ and Spo₂ as well as limits of agreement when Sao₂ values were < 80%. Additionally, in the ideal situation, Spo₂ should have been compared with Sao₂ values determined by use of a co-oximeter rather than with a calculated value; however, this instrument was not available to the investigators of the present study. Therefore, it is possible that some error in accuracy may occur owing to the use of a calculated, rather than measured, Sao₂ via co-oximetry.

Finally, although the benefits of the noninvasive and continuous ability to monitor Petco₂ and Spo₂ are clear, the inherent limitations of the actual instruments (ie, the capnograph and pulse oximeter) must be recognized. Sidestream capnography slightly increases airway resistance and also draws 125 to 500 mL of gas/min from the patient, but these factors would be negligible in most foals.³⁸ Pulse oximetry has technical limitations, including a limited ability of the instrument to detect an arterial pulse in patients with impaired arterial perfusion from shock, hypothermia, or hypovolemia. Motion artifact in conscious foals is also a common limitation. Clinicians must realize that accuracy of the instrument deteriorates when Sao₂ is < 80% and that dyshemoglobinemias (ie, carboxyhemoglobin and methemoglobin) and the use of diagnostic dyes (ie, methylene blue) will provide erroneous results.^2,12,13 Furthermore, Sao₂ is an estimate of Pao₂, and because of the sigmoid shape of the oxygen dissociation curve, large changes in Pao₂ may occur at the upper portions of the curve whereas minimal changes are observed in Sao₂. Thus, a patient, especially one receiving supplemental oxygen, may have a dramatic decrease in Pao₂ with only a minimal decrease in Spo₂. The oxygen dissociation curve may also shift as a result of increases or decreases in pH or Paco₂; thus, Spo₂ should be interpreted in light of the patient's blood pH and Paco₂.

End-tidal partial pressure of carbon dioxide and Spo₂ have been used as adequate methods of estimating and monitoring Paco₂ and blood oxygenation, respectively, in infants and adults.^2,11,39,40 Results of the study reported here suggested that Petco₂ can also be used in neonatal foals when assessment and monitoring of Paco₂ is necessary. Determination of pulse rate with a reflectance probe was reliable in this study, and Spo₂ measurements had acceptable limits of agreement with Sao₂. However, pulse oximetry underestimated Sao₂ in this study. Clinicians should realize the limitations of this study and be advised that Petco₂ and Spo₂ should not replace the judicious use of direct measurement of Paco₂ and Pao₂ via arterial blood gas analysis, especially when marked changes in Petco₂ or Spo₂ are observed.