This study of 15 animals presents physiological variables in moose anesthetized with etorphine-acepromazine-xylazine. To the best of our knowledge, this type of evaluation has not previously been reported for anesthetic protocols in moose. This study documented hypoxemia, hypercapnia and acidemia in moose immobilized with this combination.
Although the mean induction time for the 12 moose immobilized with one dart in our study was acceptable, it was over 2 minutes longer than the 4.4 ± 2.6 minutes reported in etorphine-immobilized moose . Pulse and rectal temperature did not change over time and were within acceptable ranges for this species. Guidelines for cervid anesthesia include taking corrective measures when a rectal temperature over 40°C or a heart rate under 30 beats per minute is observed .
Although the moose were kept in sternal recumbency and snow was cleared from around the nose, the position with the head lowered, may have added to the drug-induced hypoxemia seen in this study. In moose immobilized with etorphine alone, moose were in sternal recumbency [1, 21] with the head raised. Adding xylazine to opioids is not recommended in moose  as it results in a deeper immobilization, affecting the positioning (lateral without deep snow, head down) [1, 2, 22] and resulting in an increased risk of adverse effects including lower hemoglobin oxygen saturation measured by pulse oximetry (J. M. Arnemo, unpublished data) regurgitation and risk of pneumonia [1, 22] and higher mortality . Opioids, such as etorphine, produce dose-dependent respiratory depression, primarily by causing the respiratory center of the brain stem to be less responsive to increased PaCO2. The responsiveness to PaCO2 is further decreased by coadministered sedatives or other anesthetic agents including phenothiazines , such as acepromazine. Xylazine which when used alone, causes a dose-dependent decreased responsiveness to CO2 that is further compounded when combined with opioids . In sheep, xylazine was shown to cause pulmonary edema resulting in hypoxemia and lung tissue damage .
Moderate to severe hypoxemia has also been documented in other ruminants anesthetized with alpha-2 combinations including wood bison (Bison bison) , mule deer (Odocoileus heminus) [28, 29], wapiti (Cervus canadensis) [29, 30] and white tailed-deer (Odocoileus virginianus) . Hypoxemia was also found in cases where alpha-2 combinations were used in combination with opioids [28, 30]. The hypoxemia seen in this study as in studies of other ruminants, indicates that oxygen supplementation is indicated in these species. In a study of nine wapiti immobilized with xylazine-tiletamine-zolazepam, all were initially hypoxemic and in all, the hypoxemia resolved after administration of 10 L/minute of nasal oxygen for only five minutes . A study comparing nasal oxygen and medical air supplementation in wapiti before and during anesthesia with carfentanil and xylazine found that wapiti receiving 10 L/minute of oxygen had a significantly faster induction and recovery, less hypoxemia, less rigidity and movement, but more apnea, hypercapnia and acidosis . A review of alpha-2 agonist and hypoxemia concluded that hypoxemia in large ruminants such as cattle are primarily due to hypoventiliation and perfusion mismatching due to recumbency whereas sheep given xylazine can develop pulmonary edema . Evaluation of oxygen flow rates necessary to correct hypoxemia is needed for moose and other species.
The hypercapnia noted indicates hypoventilation, which also causes hypoxemia . Hypercapnia has been documented during anesthesia in a number of ruminants including wood bison , mule deer [28, 29] and wapiti [29, 30]. In a study comparing oxygen and medical air supplementation in wapiti, both groups had increasing PaCO2 over time, but this was significantly higher in the group receiving oxygen . Under ordinary conditions, increased PaCO2 stimulates and increases central respiratory drive and severely decreased PaO2 can also stimulate increased ventilation , however anesthetics depress the ventilatory response initiated by increased PaCO2. When increasing FiO2 and therefore PaO2 in carfentanil-xylazine immobilised elk a significantly increased PaCO2 was observed which is highly indicative that hypoxemia in the Elk breathing pure air had resulted in increased ventilatory drive . Hypercapnia and decreased pH also cause a right shift in the oxygen-hemoglobin dissociation curve, increasing the unloading of oxygen at tissues, enhancing oxygen delivery . Both etorphine and xylazine are likely contributing to the hypoventilation and intrapulmonary causes of hypoxemia and resulting hypoxemia and hypercapnia. As neither the hypercapnia nor hypoxemia changed with time, this indicates continued respiratory depression.
PAO2 are mostly governed by uptake of oxygen by pulmonary capillary blood and replacement by alveolar ventilation. Normal values for PAO2 for normal animals at sea level are around 13 kPa . The initial PAO2 in this study was 11.3 ± 1.0 (9.8-13.2) kPa. P(A-a)O2 was 3.0 ± 1.4 (0.7-5.6) kPa (Normal is generally less than 2 kPa with over 3.3 considered abnormal ) indicating that intrapulmonary problems like V/Q mismatch, physiological shunting or diffusion impairment could be contributing factors. Within the study group, we found large variations between animals ranging from normal function to animals with a markedly high P(A-a)O2.
The hypoxemia seen in all animals could be due to a variety of possible causes including low inspired O2 pressure (altitude), hypoventilation, V/Q mismatch, pulmonary shunting or diffusion limitations. Barometric pressure ranged from 694 to 708 mmHg, so low barometric  pressure would not be expected to contribute significantly to the hypoxemia observed. The spread of P(A-a)O2 a would indicate most moose have a pulmonary problem in addition to likely hypoventilation. A future evaluation of the effect of positioning (head uphill vs. downhill vs. flat ground) is warranted, however, these large animals can be difficult to reposition beyond moving from lateral to sternal recumbency.
We found a marked acidosis, both respiratory and metabolic. The metabolic part of the acidosis improved with time, reflected in a significantly increased pH and decreased lactate and increased BE in the second sample. The severe lactic-acidemia decreased significantly over time, indicating either decreasing lactate production, increased lactate metabolism or a combination of these. The mean lactate levels in arterial blood in the present study were slightly higher than the mean venous lactate levels in etorphine-immobilized moose reported by  who found significantly lower lactic acid levels in animals with longer induction times and with increased time between darting and sampling. That study found a plasma lactate of 9.3 ± 2.1 (2.9-12.5) mmol/L and blood was sampled at 11.0 ± 4.1 (6.0-19.9) minutes after darting. The moose in the current study had both longer induction times, a later sampling time and higher lactate than found in etorphine-immobilized moose . Furthermore, lactate is normally higher in venous samples than in arterial . This indicates that moose immobilized with etorphine-xylazine-acepromazine had higher lactate levels than moose immobilized with etorphine alone.
Anion gap decreased, likely caused by the lactic acidosis. K increased between the samples in spite of an increase in pH. As an increased pH will usually decrease K, the increased K likely reflects that K has leaked out of damaged cells, possibly muscular cells. The decrease in Hb and Hct could be a result of sequestration of erythrocytes in the spleen or increased intravascular fluid volume due to diffusion of interstitial fluid into the vascular space. This usually happens during anaesthesia due to vasodilatation and decreased blood pressure, which is consistent with xylazine and acepromazine anesthesia in some ruminants, however the etorphine usually causes increased blood pressure.