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Arterial blood was collected from 25 clinically normal horses immediately before and serially throughout the first hour of halothane oxygen anaesthesia. Blood was analysed for oxygen and carbon dioxide partial pressure (PaO2, PaCO2). Measurements of inspired oxygen concentration during anaesthesia permitted direct correlation with blood gases. Horses were divided arbitrarily into two groups based on their age: two to seven years, n = 15; over seven years, n = 10. Average (+/- sd) PaO2 and PaCO2 was 14.1 +/- 1.5 kPa (106 +/- 11 mmHg) and 5.9 +/- 0.6 kPa (44.4 +/- 4.4 mmHg) respectively in conscious, young horses and 14.0 +/- 0.7 and 5.8 +/- 0.5 kPa (105 +/- 5 and 43.3 +/- 3.8 mmHg) respectively in conscious older horses. Arterial oxygen tension decreased to 9.3 +/- 1.0 and 8.5 +/- 1.4 kPa (69.6 +/- 7.8 and 63.7 +/- 10.4 mmHg) in young and older air breathing horses respectively immediately following intravenous anaesthetic induction, recumbency and orotracheal intubation. At this time, PaCO2 was 6.5 +/- 0.5 and 6.0 +/- 0.7 kPa (48.7 +/- 3.5 and 45.1 +/- 4.9 mmHg) respectively. By 30 mins after the start of halothane in oxygen (6 litres/min) anaesthesia PaO2 increased to a maximum in both study groups. Arterial PCO2 increased steadily during anaesthesia and 60 mins after induction PaCO2 was 10.5 +/- 2.4 kPa (78.5 +/- 17.8 mmHg) in the younger horses and 9.2 +/- 1.6 kPa (68.8 +/- 11.8 mmHg) in the older horses. During inhalation anaesthesia PaO2 tended to be greater at comparable time periods in the younger horses despite a slightly greater degree of hypoventilation.

We studied the interaction of meperidine and halothane in 24 unmedicated, spontaneously breathing dogs. Intramuscular (i.m.) injections of meperidine, 2.75 mg/kg, 5.5 mg/kg and 11.0 mg/kg reduced the minimal alveolar concentration (MAC) of halothane required for anaesthesia. The magnitude and duration of MAC depression were dose related. Plasma meperidine concentrations following an i.m. injection of 2.75 mg/kg were lower in the awake, unsedated dogs than in the dogs anaesthetized with halothane.

The minimal alveolar concentration of anesthetic required to prevent gross purposeful movement in response to electrical stimulation of oral mucous membranes was determined in horses for 3 agents. Equipotent concentrations of enflurane were 2.12 volumes %; of halothane, 0.88 volumes %; and of isoflurane, 1.31 volumes +. The alveolar concentration required to produce at least 60 seconds of apnea was also determined for these agents. From these data and the minimal alveolar concentration information, anesthetic indices were determined for each agent. The indices for enflurane, halothane, and isoflurane were 2.26, 2.60, and 2.33, respectively.

Cardiopulmonary effects of prolonged, constant-alveolar-dose halothane (HAL) and methoxyflurane (MOF) in O2 anesthesia on spontaneously breathing dogs were determined. One hour after anesthetic induction, end-tidal concentration was set at 1.04% HAL or 0.28% MOF [each representing 1.2 minimum alveolar concentration (MAC) for dogs] and maintained for 7 h. No time-related changes were associated with MOF. However, HAL significantly (P less than 0.05) elevated cardiac output (Q) from 2 to 7 h by increasing stroke volume; mean aortic pressure (MAP) also increased with time (P less than 0.05 beginning at 5 h). Four of these dogs were studied again at least 3 wk later at a constant end-tidal dose of 1.48% HAL in O2 (1.7 MAC). Q and MAP were lower initially during 1.7 MAC than during 1.2 MAC but not after 2 h of anesthesia. The greater HAL dose initially depressed ventilation and elevated arterial partial pressure of CO2 (PaCO2) compared with the lower dose. PaCO2 continued to increase with duration of 1.7 MAC HAL, as did results of ventilatory gas volume and flow measurements.

Circulatory and respiratory function was monitored in nonmedicated, spontaneously breathing horses (n = 7) immediately before, during, and 1 hour after 85 +/- 4.1 (X +/- SEM) minutes of constant 1.57% isoflurane in O2 anesthesia. Comparison of values during anesthesia with those obtained while horses were awake revealed a significant (P less than 0.05) decrease in arterial blood pressure that was related to a slight, but insignificant, decrease in cardiac output and peripheral vascular resistance. Although isoflurane anesthesia and recumbency resulted in a significant (P less than 0.05) decrease in stroke volume, cardiac output did not decrease significantly because heart rate tended to increase. Isoflurane and recumbency also significantly (P less than 0.05) increased PaCO2, peak expiratory gas flow, total expiratory time, and PCV and significantly decreased PaO2, minute expired ventilation, and the ratio of peak inspired to expired gas flow. Differences imposed by isoflurane anesthesia were reversed by 1.5 hour after anesthesia.

Effects of body position and type of ventilation were determined on arterial blood gases (PaO2, PaCO2) and pH during and immediately following clinical halothane anesthesia in 36 young, physically conditioned horses. Horses in dorsal recumbency had a lower PaO2 than did similarly breathing horses in a lateral position. Predictably controlled positive-pressure ventilation inproved arterial oxygenation and permitted maintenance of a normal PaCO2. Most horses, regardless of type of ventilation and operative body positioning, were hypoxemic in the immediate postanesthetic period.

Xylazine given IV at doses of 0.5, 1.0, and 1.5 mg/kg to mares caused a significant (P less than 0.05) dose-related increase in serum glucose concentration and urine volume. Serum glucose concentrations as much as 150 mg/dl were recorded in mares after they were given the largest xylazine dose. The greatest urine volume, similar to changes in peak glucose concentration, always occurred during the first hour after dosing with xylazine and averaged 1.82, 3.93, and 5.68 ml/kg/hour after the 0.5-, 1.0-, and 1.5-mg/kg doses, respectively, were given. Urine osmolality and specific gravity were significantly (P less than 0.05) inversely related to urine volume. Although serum glucose concentrations were significantly increased above those measured after IV injection of saline solution, significant glucosuria was not detected.

Successful anesthetic management of food animals depends on knowledge of basic principles and techniques of anesthesia common to most species. When specifically considering food animals, additional emphasis is directed toward animal size, temperament, and anatomy. Respiratory failure induced by a variety of mechanisms is a major complication of special importance in ruminants. Problems relate especially to difficulty of endotracheal intubation, inhalation of saliva and rumen contents, and reduced lung gas volume caused by abdominal organ (especially rumen)-induced cranial diaphragmatic displacement. When evaluating swine for anesthesia, specific additional management considerations include accessibility of peripheral blood vessels, ease of endotracheal intubation, and porcine malignant hyperthermia.

To determine the effect of nitrous oxide on the body's response to venous carbon dioxide (CO2) embolization, the authors compared changes in mean pulmonary arterial pressure (MPAP) following intravenous injections of CO2 in pentobarbital-anesthetized dogs breathing 100 per cent oxygen (O2) or nitrous oxide--oxygen, 79:21 per cent (N2O). When CO2 was infused intravenously in seven dogs at a rate of 3 ml/kg/min the volume of injected CO2 needed to increase MPAP to 40 per cent above control during breathing of O2 was approximately 5.5 times the volume necessary during inhalation of N2O. In a second group of eight dogs, breathing N2O, compared with O2 or air, resulted in a significantly greater increase and duration of increase in MPAP following a bolus injection of CO2 of 20, 40 or 80 ml. The data suggest that breathing nitrous oxide intensifies and prolongs the effect of CO2 bubbles in blood. While the magnitude of insult following intravenous injection of CO2 is about 6.5 times less than that for a similar volume of air, avoidance of nitrous oxide should be considered in management of patients in whom CO2 embolism is possible.

Because of the calf's popularity as an experimental animal and its often noted sensitivity to anesthetics and anesthesia, the potency of halothane was studied in eight, young (x = 5.85 weeks), healthy, male Holstein-Friesian calves. The minimal alveolar halothane-O2 concentration (MAC) which just prevented calf movement in response to a tail clamp was 0.76 +/- SEM 0.03 vol% and is less than predictions based on studies in man. The addition of 50% N2O to inspired gases decreased the halothane MAC to 0.59 +/- 0.03%. In the absence of common modifying factors of anesthesia, halothane-O2 caused cardiopulmonary depression in these calves in proportion to anesthetic dose. Only two (total protein and albumin) of 17 selected blood clinical biochemical values were significantly (P less than 0.05) altered from base line within seven days of anesthesia, indicating insults to major organ systems did not occur.

The acute and long-term quantitative and qualitative effects of halothane anesthesia on equine platelet performance were studied in fourteen horses. Horses were anesthetized with only halothane in O2 for about 8.0 MAC hours. Platelet numbers declined during the anesthetic period but returned to normal within 24 h. Platelet aggregation was significantly diminished during the anesthetic period and for up to 4 days after anesthesia. A period of hyperaggregability occurred at the 7th day.

The precision of isoflurane delivery from 4 vaporizers designed and calibrated for halothane was studied. Isoflurane concentration in oxygen (O2) was determined for various vaporizer dial settings (0 to maximum) and O2 flow rates (0.375 to 15 L/min). The effects on vaporizer output of time (settings constant for up to 15 minutes), ambient temperature (15, 22, 30 C), and conditions simulating intermittent positive-pressure ventilation were also studied. The performance of the 4 halothane-specific vaporizers with isoflurane was qualitatively similar and was within the range expected as normal accuracy for halothane delivery in these same vaporizers. At room temperature, isoflurane concentrations were generally greater than dialed percentages with low carrier gas flows and were less than dialed percentages at higher gas flows for most vaporizers. The relationship of halothane output relative to isoflurane measured during similar conditions fits arithmetic coordinates well. Compared with concentrations of halothane, slightly higher concentrations of isoflurane were delivered from 3 halothane vaporizers studied (av 14%, 15%, and 8%). Temporal changes in delivered isoflurane concentration at room temperature were relatively small at low dial and carrier gas-flow rate settings. However, as gas-flow rate and vaporizer dial settings increased, vaporizer output decreased with time. Alterations in accuracy of isoflurane delivery by 1 vaporizer with temperature changes were most pronounced at the higher gas-flow rates, higher vaporizer dial settings, and lowest temperature. There was little effect of simulated positive-pressure breathing on vaporizer output at peak inspired circuit pressures less than 12 mm of Hg. Use of halothane-specific vaporizers to deliver isoflurane has advantages and disadvantages which must be evaluated individually. The delivery of isoflurane by halothane-specific vaporizers is not recommended by anesthetic and vaporizer manufacturers.

The cardiovascular effects of equipotent (minimum alveolar concentration; MAC) doses of halothane versus halothane plus 25% N2O (H25N2O) in spontaneously breathing dogs do not differe except that nitrous oxide increased mean arterial pressure (AP) and decreased arterial oxygen partial pressure (PAO2). When 75% nitrous oxide was added to halothane anesthesia, AP, mean pulmonary artery pressure (PAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and left ventricular work (LVW) increased and PAO2 and hemoglobin saturation decreased. Arterial oxygen tensions below 80 torr were common at moderate and deep anesthetic levels of halothane plus 75% N2O (H75N2O). The specific contribution of N2O, hypoxemia, hypercapnia, or temporal recovery (or a combination of these) in producing cardiovascular stimulation were not determined.

High frequency jet ventilation (HFJV) is a recently developed mode of ventilation that delivers small tidal volumes at frequencies greater than 60 cycles per min via an injection catheter to the animal's airway. The construction of a high frequency jet ventilator suitable for use in adult horses is described. The effectiveness of this ventilator in maintaining normal arterial blood-gas tension was evaluated in five healthy adult horses. The horses were anaesthetised with intravenous acetylpromazine, guaifenesin, and thiamylal, positioned in lateral recumbency and baseline measurements were made during spontaneous ventilation. The horses were then paralysed with succinylcholine and ventilated for at least 20 mins with HFJV. Air was delivered from the ventilator to the animal by a polyethylene tube. The tip of this tube remained within and approximately 30 cm from the cuffed end of a standard 30 mm internal diameter large animal orotracheal tube. Frequency of flow interruption was 3 Hz with a constant source pressure of 275 kPa and an inspiratory to expiratory ratio of approximately 1:2.6. Gas delivery to the horse, as estimated with a resonator system was approximately 2 litres/breath. During HFJV, arterial carbon dioxide tension was significantly reduced and arterial oxygen tension significantly increased above measurements made when the horses were spontaneously breathing air.

Circulatory and respiratory responses to graded increases in alveolar concentrations of enflurane were investigated in unpremedicated healthy dogs during conditions of spontaneous and controlled ventilation. The minimal alveolar concentration (MAC) of enflurane that prevented movement in response to a standard painful stimulus was determined for each dog and averaged 2.06 vol%. In these studies, enflurane produced cardiopulmonary depression in proportion to the alveolar dose. The average end-tidal enflurane concentration that produced at least 60 s of apnea was 5.29 vol% (ie, MAC 2.57). A comparison of these data with previous studies in dogs indicates that equipotent concentrations of enflurane are at least as depressant to the cardiopulmonary system as halothane and isoflurane.

Cardiopulmonary effects of spontaneous, assisted, and controlled ventilatory modes were determined with 6 young, healthy geldings anesthetized with halothane at a constant dose (1.3 minimum alveolar concentration). All horses were in lateral recumbency, and all modes of ventilation were studied at least once during each anesthetic exposure. Cardiac output did not differ between spontaneous and assisted ventilation modes, but both modes were associated with significantly (P less than 0.05) higher cardiac output than that with controlled ventilation. The PaCO2 differed significantly (P less than 0.01) between all modes of ventilation. Although controlled ventilation maintained a normal PaCO2, assisted ventilation reduced PaCO2 as compared with spontaneous ventilation with less cardiovascular depression than that with controlled ventilation. Mixed venous O2 tensions were higher with spontaneous and assisted ventilation modes than with controlled ventilation. Except for shorter inspiratory time and smaller inspiratory/expiratory ratio associated with spontaneous ventilation, there were no ventilatory mode-related effects on ventilatory variables.

Cardiovascular effects of venous alveolar concentrations of halothane in oxygen were studied in 8 young, healthy horses under conditions of constant arterial carbon dioxide tension. The alveolar concentration of halothane was expressed as a multiple of the minimal alveolar concentration (MAC) which was known for each animal. Increasing alveolar halothane concentrations to MAC 2.0 resulted in a progressive and significant (P less than 0.05) decline in systemic arterial pressure and left ventricular work. Cardiac output decreased between MAC 1.0 and MAC 2.0 as a result of a significant (P less than 0.05) decrease in stroke volume. Heart rate, total peripheral resistance, pulmonary artery pressure, hematocrit, plasma protein concentration, arterial oxygen tension, and arterial pH remained constant over the same range of anesthetic dosages. Continuation of anesthesia, spontaneous ventilation, and the accompanying rise in arterial carbon dioxide tension and electrical stimulation of the horse's oral mucous membranes produced varying degrees of stimulation of cardiovascular function at MAC 1.5.

The slow rate of change of inspired halothane concentration which results in a conventional large animal circle anesthetic delivery system when low carrier gas flow rates are used was confirmed, using a model system. To obtain a 63% change in inspired halothane concentration in the 32-L large animal circle anesthetic machine at fresh gas inflow rates of 3, 6, and 12 L/minute required 10.7, 5.3, and 2.7 minutes, respectively. At a given inflow rate, increasing the rebreathing bag size from 20 to 40 L prolonged the time for equilibration between the gas flowing into the anesthetic circuit and the inspired gas. The extent to which an adult horse further slowed the rate of rise of inspired anesthetic concentration was also demonstrated.

Sequelae of routine orotracheal intubation under clinical conditions were characterised in 38 healthy horses presented at three veterinary medical teaching hospitals. Four of these were necropsied and their tissues studied histologically. To minimise variation, 30 mm id cuffed silicone endotracheal tubes or Cole cuffless tubes were used in all patients. Fibreoptic endoscopic examination of upper respiratory and tracheal areas was accomplished pre-intubation, immediately post extubation and after 24 h. Endoscopy revealed that intubation was associated with laryngeal and/or tracheal lesions in all horses. Observations included abundant tracheal mucus, epithelial ecchymoses, basement membrane haemorrhage and mucus covered diphtheritic membrane plaques. Histological examination of lesions from the upper respiratory system of the four necropsied horses confirmed that the damage was comparable to that associated with tracheal intubation and reported in other species.