The effect of hypercapnia on the arrhythmogenic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an end-tidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [Pa(CO2)] = 35 to 45 mm of Hg), at hypercapnia (Pa(CO2) = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 micrograms/kg of body weight/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate, to the nearest 0.25 micrograms/kg/min, at which 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean +/- SD) during hypercapnia (1.04 +/- 0.23 micrograms/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 +/- 0.38 micrograms/kg/min), whereas the ADE after return to normocapnia (1.17 +/- 0.22 micrograms/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (Pa(O2)) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

This study was designed to test analgesia, duration, and cardiovascular changes induced by meperidine (MEP) and oxymorphone (OXY) following methoxyflurane (MOF) and halothane (HAL) anesthesia. Eight healthy dogs were given atropine and acepromazine, and anesthesia was induced with thiamylal and maintained with 1.5 minimal alveolar concentration of MOF or HAL for 1 hour during controlled ventilation. Eight treatments were given with each anesthetic: 3 with MEP (0.5, 1.0, and 2.0 mg/kg, IV), 3 with oxymorphone (OXY; 0.05, 0.1, and 0.2 mg/kg, IV), and 2 placebos with sterile water. Test drugs were given at the end of anesthesia when early signs of recovery were evident. Minimal threshold stimulus/response nociception was assessed by use of an inflatable soft plastic colonic balloon. Blood pressures and pulse rate were measured with a noninvasive monitor. Meperidine and OXY were found to be effective analgesics and could be reversed with naloxone. Intravenous administration of 2.0 mg of MEP/kg provided analgesia for 36 +/- 6 minutes and 39 +/- 15 minutes after MOF and HAL, respectively. In contrast, OXY was effective at all 3 doses with effects of IV administration of 0.2 mg of OXY/kg lasting 154 +/- 13 minutes and 152 +/- 12 minutes, after MOF and HAL, respectively. Analgesia could not be demonstrated after anesthesia for acepromazine, MOF, or HAL. Blood pressure was not changed by either anesthetic nor was it influenced by MEP or OXY. Pulse rate was significantly depressed by the higher doses of OXY following HAL, but was not changed by MEP following either anesthetic. This study demonstrated the longer duration of analgesia of OXY. In addition, we could not find that analgesia was provided by either MOF or HAL following recovery from anesthesia.

Hemodynamic effects of spontaneous ventilation, intermittent positive-pressure ventilation (IPPV), and high-frequency oscillatory ventilation (HFOV) were compared in 6 dogs during halothane anesthesia. Anesthesia was induced with IV thiamylal Na and was maintained with halothane (end-tidal concentration, 1.09%). During placement of catheters, dogs breathed spontaneously through a conventional semiclosed anesthesia circuit. Data were collected, and dogs were mechanically ventilated, using IPPV or HFOV in random order. Ventilation was adjusted to maintain PaCO2 between 38 and 43 mm of Hg during IPPV and HFOV. Cardiac index, aortic blood pressure, and maximum rate of increase of left ventricular pressure were significantly (P less than 0.05) less during HFOV than during spontaneous ventilation, whereas right atrial and pulmonary artery pressure were significantly greater during HFOV than during spontaneous ventilation. During IPPV, only the maximum rate of increase of left ventricular pressure was significantly less than that during spontaneous ventilation.

Effects of ketamine, xylazine, and a combination of ketamine and xylazine were studied in 12 male Pekin ducks (7 to 12 weeks old; mean [+/- SD] body weight, 3.1 +/- 0.3 kg). After venous and arterial catheterization and fixation of a temperature probe in the cloaca, each awake duck was confined, but not restrained, in an open box in a dimly lit room. Blood pressure and lead-II ECG were recorded. Three arterial blood samples were collected every 15 minutes over a 45-minute period (control period) and were analyzed for pHa, Paco2 and Pao2. After the control period, each duck was assigned at random to 1 of 3 drug groups: (1) ketamine (KET; 20 mg/kg of body weight, IV), (2) xylazine (XYL; 1 mg/kg, IV), and (3) KET + XYL (KET 20 mg/kg and XYL, 1 mg/kg; IV). Measurements were made at 1, 5, 10, 15, 30, 45, 60, and 90 minutes after drug administration. All ducks survived the drug study. Cloacal temperature was significantly (P less than or equal to 0.05) increased above control cloacal temperature at 90 minutes after the administration of ketamine, and from 10 through 90 minutes after administration of ketamine plus xylazine. In ducks of the KET group, pHa, Paco2, and Pao2, remained unchanged after administration of the drug. In ducks of the XYL group, pHa and Pao2 decreased significantly (P less than or equal to 0.05) from control values for all time points up to and including 15 minutes after drug administration. In ducks of the KET + XYL group, pHa and Pa02 were significantly (P less than or equal to 0.05) decreased at all time points up to and including 45 and 15 minutes, respectively, after administration of the drugs. In ducks of the XYL group, Paco2 increased significantly (P less than 0.05) during the first 15 min. after drug administration, and for 45 min. after administration of KET + XYL. Results indicated that ketamine when given alone to ducks, was not associated with pulmonary depression.