Use of Naloxone to Reverse Carfentanil Citrate-Induced Hypoxemia and Cardiopulmonary Depression in Rocky Mountain Wapiti (Cervus elaphus nelsoni)
IAAAM Archive
Anneke Moresco1, DVM, MS; R. Scott Larsen1, DVM, MS; Jonathan M. Sleeman1, VetMB, MRCVS; Margaret A. Wild2, DVM; James S. Gaynor1, DVM, MS
1Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA; 2Colorado Division of Wildlife, Fort Collins, CO, USA; Present address: Farm Animal Health and Resource Management, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA; Present address: Environmental Medicine Consortium, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA


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.

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Anneke Moresco, DVM, MS

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