Use of Naloxone to Reverse Carfentanil Citrate-Induced Hypoxemia and Cardiopulmonary Depression in Rocky Mountain Wapiti (Cervus elaphus nelsoni)
Potent opioids such as carfentanil and etorphine are commonly used for hoofstock anesthesia because they
provide a rapid induction.2,3 However, they can have serious side effects that include profound hypoxemia,
cardiopulmonary depression, bradycardia, and decreased gastrointestinal motility.4 The purpose of this study was to
investigate the use of naloxone to reverse or partially reverse these effects while maintaining adequate anesthesia.1
Eight healthy female Rocky Mountain wapiti (Cervus elaphus nelsoni, mean age ± SD, 10.1 ± 2.6 yr; mean weight
± SD, 265 ± 26 kg) were used in a crossover study to compare the respiratory and cardiovascular effects of i.m.
carfentanil-xylazine-placebo (CXP) and i.m. carfentanil-xylazine supplemented with i.v. naloxone (CXN). The study was performed
during April and May 1999 in Fort Collins, CO (elevation 1495 m and Patm = 640 mm Hg).
Anesthesia was induced and maintained with i.m. carfentanil (10 µg/kg; Wildnil, Wildlife Pharmaceuticals,
Fort Collins, CO 80525 USA) and xylazine (0.1 mg/kg; Cervizine, Wildlife Pharmaceuticals, Fort Collins, CO 80525 USA), dosages
previously reported to be effective in wapiti.2,3 Mean induction time was 3.7 ± 0.9 min. After an i.v. catheter and
monitoring equipment were placed, animals were administered an i.v. bolus of naloxone (2 µg/µg carfentanil; Naloxone HCl
injection, Elkins-Sinn, Cherry Hill, NJ 08003 USA) or an equivalent volume of placebo (normal saline). Arterial blood was obtained
directly from an arterial catheter and a portable blood gas analyzer was used to measure arterial blood oxygen
(PaO2) and carbon dioxide (PaCO2) partial pressures.
At the time of instrumentation, animals were profoundly hypoxemic (PaO2 was 23.0 ±
4.1 mm Hg; mean ± SD). Oxygenation values increased to 50.2 ± 7.3 mm Hg (mean ± SD) at t = 10 min. after naloxone
administration; mean PaO2 of placebo-treated animals did not change significantly over time. The difference
in PaO2 between treatment groups was significant for all measurements from t = 10 to t = 30 min, however, the
PaO2 in the CXN group gradually returned toward baseline levels over time (PaO2 = 34.61
± 4.7 at t = 30 min). Three animals in the placebo group exhibited electrocardiogram (ECG) changes suggestive of myocardial
hypoxia. Hypoxemia is likely to have been due to multiple factors including hemodynamic alterations and lateral recumbency, in
addition to the respiratory depression induced by the opioids.
Anesthesia with carfentanil-xylazine also produced mild hypercapnia (54.3 ± 4.6 mm Hg), mild acidosis (pH
= 7.32 ± 0.04), and mild tachycardia (63.9 ± 16.7 bpm). There were significant differences (P < 0.05) in
PaO2, PaCO2, heart rate, and respiratory rate between treatment and placebo groups.
Significant differences between groups were not detected for mean blood pressure, hematocrit, or serum electrolytes.
After naloxone treatment, one animal suddenly stood and walked; all other animals remained anesthetized after
naloxone administration. Reversal of anesthesia was achieved with naltrexone (100 mg/mg carfentanil; 25% i.v. and 75% s.c.;
Trexonil, Wildlife Pharmaceuticals, Fort Collins, CO 80525 USA) and yohimbine (0.1 mg/kg; Antagonil, Wildlife Pharmaceuticals, Fort
Collins, CO 80525 USA). Reversal time was # 4 min for both groups.
This investigation documents the profound hypoxemia that is induced with carfentanil-xylazine anesthesia in
wapiti. It also demonstrates the efficacy of a bolus of naloxone as a practical method of improving oxygenation. In the wapiti of
this study, an i.v. bolus of naloxone, at a dose of 2 ? naloxone per ? (editor's note: I was not able to read
the dosage in the original pdf) carfentanil, was effective in ameliorating carfentanil-induced hypoxemia. However, the arousal of
one animal suggests that this naloxone dose may be the high-end dose for captive wapiti, that it may be more appropriate to start
with a lower dose, and that caution should be used when administering this treatment.
We acknowledge Wildlife Pharmaceuticals for providing drugs and Kendall, Sherwood-Davis, and Geck for
supplying equipment used in this investigation. We thank Drs. W.R. Lance and C. Pichet for valuable discussions. We also thank
faculty and staff of the Anesthesia Section at Colorado State University and K. T. Castle for technical assistance.
1. Drummond GB, IT Davie, DB Scott. 1977. Naloxone: Dose-dependent antagonism of respiratory
depression by fentanyl in anaesthetized patients. Br. J. Anaesth. 49: 151-154.
2. Kreeger TJ. 1996. Handbook of Wildlife Chemical Immobilization. International Wildlife
Veterinary Services, Laramie, Wyoming.
3. Miller MW, MA Wild, WR Lance. 1996. Efficacy and safety of naltrexone hydrochloride for
antagonizing carfentanil citrate immobilization in captive Rocky Mountain elk (Cervus elaphus nelsoni). J. Wildl.
Dis. 32: 234-239.
4. Wagner AE, WW Muir, BJ Grospitch. 1990. Cardiopulmonary effects of position in conscious
cattle. Am. J. Vet. Res. 51: 7-10.