Agreement between arterial partial pressure of carbon dioxide and saturation of hemoglobin with oxygen values obtained by direct arterial blood measurements versus noninvasive methods in conscious healthy and ill foals

David M. Wong Lloyd Veterinary Medical Center, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

Search for other papers by David M. Wong in
Current site
Google Scholar
PubMed
Close
 DVM, MS, DACVIM, DACVECC
,
Cody J. Alcott Lloyd Veterinary Medical Center, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

Search for other papers by Cody J. Alcott in
Current site
Google Scholar
PubMed
Close
 DVM, DACVIM
,
Chong Wang Department of Production Animal Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

Search for other papers by Chong Wang in
Current site
Google Scholar
PubMed
Close
 PhD
,
Jennifer L. Bornkamp Lloyd Veterinary Medical Center, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

Search for other papers by Jennifer L. Bornkamp in
Current site
Google Scholar
PubMed
Close
 DVM
,
Jessica L. Young Lloyd Veterinary Medical Center, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

Search for other papers by Jessica L. Young in
Current site
Google Scholar
PubMed
Close
 DVM
, and
Brett A. Sponseller Lloyd Veterinary Medical Center, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50011.

Search for other papers by Brett A. Sponseller in
Current site
Google Scholar
PubMed
Close
 DVM, PhD, DACVIM

Abstract

Objective—To investigate tissue diffusion of anesthetic agent following administration of low palmar nerve blocks (LPBs) in horses.

Design—Randomized clinical trial.

Animals—12 adult horses.

Procedures—In 9 horses, mepivacaine hydrochloride–iohexol (50:50 dilution) injections were administered bilaterally (2 or 4 mL/site) to affect the medial and lateral palmar and palmar metacarpal nerves (4 sites). Lateral radiographic views of both metacarpal regions were obtained before and at 5, 15, 30, 60, 90, and 120 minutes after block administration; proximal and distal extents of contrast medium (and presumably anesthetic agent) diffusion from palmar and palmar metacarpal injection sites were measured and summed to determine total diffusion. Methylene blue solution was injected in forelimbs of 3 other horses that were subsequently euthanized to determine the potential route of anesthetic agent diffusion to the proximal suspensory ligament region.

Results—Mean extents of proximal and total contrast medium diffusion were 4.0 and 6.6 cm, respectively, for the palmar metacarpal nerves and 4.3 and 7.1 cm, respectively, for the palmar nerves. Subtle proximal diffusion secondary to lymphatic drainage was evident in 17 of the 18 limbs. Contrast medium was detected in the metacarpophalangeal joint or within the digital flexor tendon sheath in 8 and 7 limbs, respectively. In the cadaver limbs, methylene blue solution did not extend to the proximal suspensory ligament region.

Conclusions and Clinical Relevance—In horses, LPBs resulted in minimal proximal diffusion of anesthetic agent from the injection sites. Limbs should be aseptically prepared prior to LPB administration because inadvertent intrasynovial injection may occur.

Abstract

Objective—To investigate tissue diffusion of anesthetic agent following administration of low palmar nerve blocks (LPBs) in horses.

Design—Randomized clinical trial.

Animals—12 adult horses.

Procedures—In 9 horses, mepivacaine hydrochloride–iohexol (50:50 dilution) injections were administered bilaterally (2 or 4 mL/site) to affect the medial and lateral palmar and palmar metacarpal nerves (4 sites). Lateral radiographic views of both metacarpal regions were obtained before and at 5, 15, 30, 60, 90, and 120 minutes after block administration; proximal and distal extents of contrast medium (and presumably anesthetic agent) diffusion from palmar and palmar metacarpal injection sites were measured and summed to determine total diffusion. Methylene blue solution was injected in forelimbs of 3 other horses that were subsequently euthanized to determine the potential route of anesthetic agent diffusion to the proximal suspensory ligament region.

Results—Mean extents of proximal and total contrast medium diffusion were 4.0 and 6.6 cm, respectively, for the palmar metacarpal nerves and 4.3 and 7.1 cm, respectively, for the palmar nerves. Subtle proximal diffusion secondary to lymphatic drainage was evident in 17 of the 18 limbs. Contrast medium was detected in the metacarpophalangeal joint or within the digital flexor tendon sheath in 8 and 7 limbs, respectively. In the cadaver limbs, methylene blue solution did not extend to the proximal suspensory ligament region.

Conclusions and Clinical Relevance—In horses, LPBs resulted in minimal proximal diffusion of anesthetic agent from the injection sites. Limbs should be aseptically prepared prior to LPB administration because inadvertent intrasynovial injection may occur.

Ill foals presented for veterinary care often require assessment of blood oxygenation and evaluation of the status of patient ventilation.1 Arterial blood gas analysis remains the gold standard for evaluation of these variables and is commonly used for this purpose to define and monitor arterial blood oxygenation and pulmonary function in ill foals. However, it can be difficult to collect arterial blood samples from foals, particularly foals with hypovolemia or in a state of circulatory shock. Other limitations and disadvantages of arteriopuncture include inadvertent collection of venous blood, hematoma formation, and poor patient cooperation. Furthermore, repeated arterial blood sample collection can result in pain and stress in foals along with vascular trauma and added client expense. In humans, capnography and pulse oximetry are noninvasive methods of assessing the Paco2 and the Sao2, respectively, as indirect measures of ventilation and oxygenation.2

In general, the Petco2 is lower than arterial values because of intrapulmonary dead-space ventilation, physiologic shunting, and variation in ventilation-to-perfusion ratios.3–6 In healthy people and small animal species, the difference between Paco2 and Petco2, also known as the Paco2–Petco2 gradient, is < 5 mm Hg.5,7,8 The correlation between Petco2 and Paco2 has been good in awake, nonintubated people and dogs.5,6,9–11 However, neither the correlation between Petco2 and Paco2 nor the evaluation of the Paco2–Petco2 gradient in conscious neonatal foals has been investigated. Similarly, numerous studies2,12 on infants have demonstrated good to excellent accuracy and reliability of Sao2 measured by use of pulse oximetry, compared with the accuracy and reliability calculated by use of arterial blood gas analysis, in the neonatal critical care setting. One study13 on foals concluded that pulse oximetry is a valuable method for assessing Sao2 in anesthetized foals. However, investigation into the usefulness and accuracy of pulse oximetry in conscious healthy and ill foals, compared with measurements calculated from arterial blood gas analysis, has not been performed.

If adequate agreement between direct and indirect measurements of Paco2 and Sao2 exists, indirect assessment of these variables in conscious foals may be helpful in the therapeutic management of ill foals and may provide a less invasive, continuous, and more affordable means of patient monitoring. Therefore, the purpose of the study reported here was to evaluate the agreement between Paco2 and Petco2 in healthy and ill spontaneously breathing nonintubated foals. In addition, the agreement between the Spo2 and Sao2 was determined. A further objective was to determine whether respiratory rate, heart rate, or rectal temperature was associated with the accuracy of capnography or pulse oximetry. We hypothesized that there would be good agreement between both Paco2 and Petco2 as well as between Spo2 and Sao2.

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 analyzera; 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 transducerb 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.

Figure 1—
Figure 1—

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

Figure 2—
Figure 2—

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

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.

Figure 3—
Figure 3—

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

Figure 4—
Figure 4—

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

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 studies3,21–23 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 studies3,22,23 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 studies3,4,21,22 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 studies5,6,9,23,29,30 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 probec 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 studies13,23,36,37 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 studies34,36 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 tongue13,23,34,36,37; 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 studies36,37 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.

ABBREVIATIONS

Petco2

End-tidal partial pressure of carbon dioxide

Sao2

Calculated saturation of hemoglobin with oxygen in arterial blood

Spo2

Saturation of hemoglobin with oxygen as measured by use of pulse oximetry

a.

Rapidlab, Bayer Heatlhcare, Rarrytown, NY.

b.

Oxisensor II RS10, Tyco Healthcare Group, Pleasanton, Calif.

c.

Passport2, Datascope Patient Monitoring, Mahwah, NJ.

References

  • 1.

    Palmer JE. Ventilatory support of the critically ill foal. Vet Clin North Am Equine Pract 2005; 21: 457486.

  • 2.

    Soubani AO. Noninvasive monitoring of oxygen and carbon dioxide. Am J Emerg Med 2001; 19: 141146.

  • 3.

    Geiser DR, Rohrbach BW. Use of end-tidal CO2 tension to predict arterial CO2 values in isoflurane-anesthetized equine neonates. Am J Vet Res 1992; 53: 16171621.

    • Search Google Scholar
    • Export Citation
  • 4.

    Hopkins SR, Bayly WM, Slocombe RF, et al. Effect of prolonged heavy exercise on pulmonary gas exchange in horses. J Appl Physiol 1998; 84: 17231730.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Kelmer E, Scanson LC, Reed A, et al. Agreement between values for arterial and end-tidal partial pressures of carbon dioxide in spontaneously breathing, critically ill dogs. J Am Vet Med Assoc 2009; 235: 13141318.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Moses JM, Alexander JL, Agus MS. The correlation and level of agreement between end-tidal and blood gas Pco2 in children with respiratory distress: a retrospective analysis. BMC Pediatr [serial online] 2009; 9:20. Available at: www.biomedcentral.com/1471-2431/9/20. Accessed Aug 10, 2010.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Schmitz BD, Shapiro BA. Capnography. Respir Care Clin North Am 1995; 1: 107117.

  • 8.

    Raffe M. Oximetry and capnography In: Wingfield W, Raffe M, eds. The veterinary ICU book. Jackson, WY: Teton NewMedia, 2002;8695.

  • 9.

    Amuchou Singh S, Singhal N. Does end-tidal carbon dioxide measurement correlate with arterial carbon dioxide in extremely low birth weight infants in the first week of life? Indian Pediatr 2006; 43: 2025.

    • Search Google Scholar
    • Export Citation
  • 10.

    Barton CW, Wang ES. Correlation of end-tidal CO2 measurements to arterial Paco2 in nonintubated patients. Ann Emerg Med 1994; 23: 560563.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Cheng KI, Tang CS, Tsai EM, et al. Correlation of arterial and end-tidal carbon dioxide in spontaneously breathing patients during ambulatory gynecologic laparoscopy. J Formos Med Assoc 1999; 98: 814819.

    • Search Google Scholar
    • Export Citation
  • 12.

    Sinex JE. Pulse oximetry: principles and limitations. Am J Emerg Med 1999; 17: 5967.

  • 13.

    Chaffin MK, Matthews NS, Cohen ND, et al. Evaluation of pulse oximetry in anaesthetised foals using multiple combinations of transducer type and transducer attachment site. Equine Vet J 1996; 28: 437445.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Smale K, Anderson LS, Butler PJ. An algorithm to describe the oxygen equilibrium curve for the Thoroughbred racehorse. Equine Vet J 1994; 26: 500502.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1986; 1: 307310.

  • 16.

    Ambalavanan N, Carlo WA. Hypocapnia and hypercapnia in respiratory management of newborn infants. Clin Perinatol 2001; 28: 517531.

  • 17.

    Jankov RP, Tanswell AK. Hypercapnia and the neonate. Acta Paediatr 2008; 97: 15021509.

  • 18.

    Giguere S, Slade JK, Sanchez LC. Retrospective comparison of caffeine and doxapram for the treatment of hypercapnia in foals with hypoxic-ischemic encephalopathy. J Vet Intern Med 2008; 22: 401405.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Vaala WE. Peripartum asphyxia. Vet Clin North Am Equine Pract 1994; 10: 187218.

  • 20.

    Bland JM, Altman DG. Measuring agreement in method comparison studies. Stat Methods Med Res 1999; 8: 135160.

  • 21.

    Meyer RE, Short CE. Arterial to end-tidal CO2 tension and alveolar dead space in halothane- or isoflurane-anesthetized ponies. Am J Vet Res 1985; 46: 597599.

    • Search Google Scholar
    • Export Citation
  • 22.

    Cribb PH. Capnographic monitoring during anesthesia with controlled ventilation in the horse. Vet Surg 1988; 17: 4852.

  • 23.

    Koenig J, McDonell W, Valverde A. Accuracy of pulse oximetry and capnography in healthy and compromised horses during spontaneous and controlled ventilation. Can J Vet Res 2003; 67: 169174.

    • Search Google Scholar
    • Export Citation
  • 24.

    Choudhury M, Kiran U, Choudhary SK, et al. Arterial-to-endtidal carbon dioxide tension difference in children with congenital heart disease. J Cardiothorac Vasc Anesth 2006; 20: 196201.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Hagerty JJ, Kleinman ME, Zurakowski D, et al. Accuracy of a new low-flow sidestream capnography technology in newborns: a pilot study. J Perinatol 2002; 22: 219225.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Short JA, Paris ST, Booker PD, et al. Arterial to end-tidal carbon dioxide tension difference in children with congenital heart disease. Br J Anaesth 2001; 86: 349353.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27.

    Taniguchi S, Irita K, Sakaguchi Y, et al. Arterial to end-tidal CO2 gradient as an indicator of silent pulmonary embolism. Lancet 1996; 348:1451.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Thys F, Elamly A, Marion E, et al. Paco(2)/etco(2) gradient: early indicator of thrombolysis efficacy in a massive pulmonary embolism. Resuscitation 2001; 49: 105108.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    McNulty SE, Roy J, Torjman M, et al. Relationship between arterial carbon dioxide and end-tidal carbon dioxide when a nasal sampling port is used. J Clin Monit 1990; 6: 9398.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 30.

    Takano Y, Sakamoto O, Kiyofuji C, et al. A comparison of the end-tidal CO2 measured by portable capnometer and the arterial Pco2 in spontaneously breathing patients. Respir Med 2003; 97: 476481.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Severinghaus JW. Water vapor calibration errors in some capnometers: respiratory conventions misunderstood by manufacturers? Anesthesiology 1989; 70: 996998.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32.

    Fletcher R, Jonson B, Cumming G, et al. The concept of dead-space with special reference to the single breath test for carbon dioxide. Br J Anaesth 1981; 53: 7788.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 33.

    Marino PL. Oximetry and capnography In: Marino PL, ed. The ICU book. Philadelphia: Lippincott Williams & Wilkins, 1998;355370.

  • 34.

    Matthews NS, Hartke S & Allen JC Jr. An evaluation of pulse oximeters in dogs, cats and horses. Vet Anaesth Analg 2003; 30: 314.

  • 35.

    Watney GC, Norman WM, Schumacher JP, et al. Accuracy of a reflectance pulse oximeter in anesthetized horses. Am J Vet Res 1993; 54: 497501.

    • Search Google Scholar
    • Export Citation
  • 36.

    Whitehair KJ, Watney GC, Leith DE, et al. Pulse oximetry in horses. Vet Surg 1990; 19: 243248.

  • 37.

    Matthews NS, Hartsfield SM, Sanders EA, et al. Evaluation of pulse oximetry in horses surgically treated for colic. Equine Vet J 1994; 26: 114116.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 38.

    Hackett TB. Pulse oximetry and end tidal carbon dioxide monitoring. Vet Clin North Am Small Anim Pract 2002; 32: 10211029.

  • 39.

    Casati A, Gallioli G, Passaretta R, et al. End tidal carbon dioxide monitoring in spontaneously breathing, nonintubated patients. A clinical comparison between conventional sidestream and microstream capnometers. Minerva Anestesiol 2001; 67: 161164.

    • Search Google Scholar
    • Export Citation
  • 40.

    Keogh BF, Kopotic RJ. Recent findings in the use of reflectance oximetry: a critical review. Curr Opin Anaesthesiol 2005; 18: 649654.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • Figure 1—

    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.

  • Figure 2—

    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).

  • Figure 3—

    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.

  • Figure 4—

    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).

  • 1.

    Palmer JE. Ventilatory support of the critically ill foal. Vet Clin North Am Equine Pract 2005; 21: 457486.

  • 2.

    Soubani AO. Noninvasive monitoring of oxygen and carbon dioxide. Am J Emerg Med 2001; 19: 141146.

  • 3.

    Geiser DR, Rohrbach BW. Use of end-tidal CO2 tension to predict arterial CO2 values in isoflurane-anesthetized equine neonates. Am J Vet Res 1992; 53: 16171621.

    • Search Google Scholar
    • Export Citation
  • 4.

    Hopkins SR, Bayly WM, Slocombe RF, et al. Effect of prolonged heavy exercise on pulmonary gas exchange in horses. J Appl Physiol 1998; 84: 17231730.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 5.

    Kelmer E, Scanson LC, Reed A, et al. Agreement between values for arterial and end-tidal partial pressures of carbon dioxide in spontaneously breathing, critically ill dogs. J Am Vet Med Assoc 2009; 235: 13141318.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 6.

    Moses JM, Alexander JL, Agus MS. The correlation and level of agreement between end-tidal and blood gas Pco2 in children with respiratory distress: a retrospective analysis. BMC Pediatr [serial online] 2009; 9:20. Available at: www.biomedcentral.com/1471-2431/9/20. Accessed Aug 10, 2010.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 7.

    Schmitz BD, Shapiro BA. Capnography. Respir Care Clin North Am 1995; 1: 107117.

  • 8.

    Raffe M. Oximetry and capnography In: Wingfield W, Raffe M, eds. The veterinary ICU book. Jackson, WY: Teton NewMedia, 2002;8695.

  • 9.

    Amuchou Singh S, Singhal N. Does end-tidal carbon dioxide measurement correlate with arterial carbon dioxide in extremely low birth weight infants in the first week of life? Indian Pediatr 2006; 43: 2025.

    • Search Google Scholar
    • Export Citation
  • 10.

    Barton CW, Wang ES. Correlation of end-tidal CO2 measurements to arterial Paco2 in nonintubated patients. Ann Emerg Med 1994; 23: 560563.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 11.

    Cheng KI, Tang CS, Tsai EM, et al. Correlation of arterial and end-tidal carbon dioxide in spontaneously breathing patients during ambulatory gynecologic laparoscopy. J Formos Med Assoc 1999; 98: 814819.

    • Search Google Scholar
    • Export Citation
  • 12.

    Sinex JE. Pulse oximetry: principles and limitations. Am J Emerg Med 1999; 17: 5967.

  • 13.

    Chaffin MK, Matthews NS, Cohen ND, et al. Evaluation of pulse oximetry in anaesthetised foals using multiple combinations of transducer type and transducer attachment site. Equine Vet J 1996; 28: 437445.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 14.

    Smale K, Anderson LS, Butler PJ. An algorithm to describe the oxygen equilibrium curve for the Thoroughbred racehorse. Equine Vet J 1994; 26: 500502.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1986; 1: 307310.

  • 16.

    Ambalavanan N, Carlo WA. Hypocapnia and hypercapnia in respiratory management of newborn infants. Clin Perinatol 2001; 28: 517531.

  • 17.

    Jankov RP, Tanswell AK. Hypercapnia and the neonate. Acta Paediatr 2008; 97: 15021509.

  • 18.

    Giguere S, Slade JK, Sanchez LC. Retrospective comparison of caffeine and doxapram for the treatment of hypercapnia in foals with hypoxic-ischemic encephalopathy. J Vet Intern Med 2008; 22: 401405.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 19.

    Vaala WE. Peripartum asphyxia. Vet Clin North Am Equine Pract 1994; 10: 187218.

  • 20.

    Bland JM, Altman DG. Measuring agreement in method comparison studies. Stat Methods Med Res 1999; 8: 135160.

  • 21.

    Meyer RE, Short CE. Arterial to end-tidal CO2 tension and alveolar dead space in halothane- or isoflurane-anesthetized ponies. Am J Vet Res 1985; 46: 597599.

    • Search Google Scholar
    • Export Citation
  • 22.

    Cribb PH. Capnographic monitoring during anesthesia with controlled ventilation in the horse. Vet Surg 1988; 17: 4852.

  • 23.

    Koenig J, McDonell W, Valverde A. Accuracy of pulse oximetry and capnography in healthy and compromised horses during spontaneous and controlled ventilation. Can J Vet Res 2003; 67: 169174.

    • Search Google Scholar
    • Export Citation
  • 24.

    Choudhury M, Kiran U, Choudhary SK, et al. Arterial-to-endtidal carbon dioxide tension difference in children with congenital heart disease. J Cardiothorac Vasc Anesth 2006; 20: 196201.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Hagerty JJ, Kleinman ME, Zurakowski D, et al. Accuracy of a new low-flow sidestream capnography technology in newborns: a pilot study. J Perinatol 2002; 22: 219225.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Short JA, Paris ST, Booker PD, et al. Arterial to end-tidal carbon dioxide tension difference in children with congenital heart disease. Br J Anaesth 2001; 86: 349353.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27.

    Taniguchi S, Irita K, Sakaguchi Y, et al. Arterial to end-tidal CO2 gradient as an indicator of silent pulmonary embolism. Lancet 1996; 348:1451.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Thys F, Elamly A, Marion E, et al. Paco(2)/etco(2) gradient: early indicator of thrombolysis efficacy in a massive pulmonary embolism. Resuscitation 2001; 49: 105108.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    McNulty SE, Roy J, Torjman M, et al. Relationship between arterial carbon dioxide and end-tidal carbon dioxide when a nasal sampling port is used. J Clin Monit 1990; 6: 9398.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 30.

    Takano Y, Sakamoto O, Kiyofuji C, et al. A comparison of the end-tidal CO2 measured by portable capnometer and the arterial Pco2 in spontaneously breathing patients. Respir Med 2003; 97: 476481.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 31.

    Severinghaus JW. Water vapor calibration errors in some capnometers: respiratory conventions misunderstood by manufacturers? Anesthesiology 1989; 70: 996998.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 32.

    Fletcher R, Jonson B, Cumming G, et al. The concept of dead-space with special reference to the single breath test for carbon dioxide. Br J Anaesth 1981; 53: 7788.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 33.

    Marino PL. Oximetry and capnography In: Marino PL, ed. The ICU book. Philadelphia: Lippincott Williams & Wilkins, 1998;355370.

  • 34.

    Matthews NS, Hartke S & Allen JC Jr. An evaluation of pulse oximeters in dogs, cats and horses. Vet Anaesth Analg 2003; 30: 314.

  • 35.

    Watney GC, Norman WM, Schumacher JP, et al. Accuracy of a reflectance pulse oximeter in anesthetized horses. Am J Vet Res 1993; 54: 497501.

    • Search Google Scholar
    • Export Citation
  • 36.

    Whitehair KJ, Watney GC, Leith DE, et al. Pulse oximetry in horses. Vet Surg 1990; 19: 243248.

  • 37.

    Matthews NS, Hartsfield SM, Sanders EA, et al. Evaluation of pulse oximetry in horses surgically treated for colic. Equine Vet J 1994; 26: 114116.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 38.

    Hackett TB. Pulse oximetry and end tidal carbon dioxide monitoring. Vet Clin North Am Small Anim Pract 2002; 32: 10211029.

  • 39.

    Casati A, Gallioli G, Passaretta R, et al. End tidal carbon dioxide monitoring in spontaneously breathing, nonintubated patients. A clinical comparison between conventional sidestream and microstream capnometers. Minerva Anestesiol 2001; 67: 161164.

    • Search Google Scholar
    • Export Citation
  • 40.

    Keogh BF, Kopotic RJ. Recent findings in the use of reflectance oximetry: a critical review. Curr Opin Anaesthesiol 2005; 18: 649654.

    • Crossref
    • Search Google Scholar
    • Export Citation

Advertisement