In: Recent Advances in Veterinary Anesthesia and Analgesia: Companion Animals, Gleed R.D. and Ludders J.W. (Eds.).

International Veterinary Information Service, Ithaca NY (www.ivis.org), Last updated: 2-Mar-2001; A1410.0301 Inhaled Anesthesia for Birds J. W. Ludders Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA. Introduction In the 1950s it was thought that birds, because of their unique pulmonary anatomy, could not be safely anesthetized with inhalant anesthetics [1]. Now, of course, we recognize that this is not the case and inhalational anesthesia is in fact a preferred method for anesthetizing birds. This article presents a brief review of the avian pulmonary system as it relates to inhalational anesthesia and a brief summary of what is currently known about inhalant anesthesia in birds. Avian Pulmonary Anatomy Trachea and Tracheal Deadspace The avian trachea is made up of complete tracheal cartilages, but the anesthetist must be aware of the tremendous variations in tracheal form and features that exist from one avian genus to another. For example, emu have an inflatable sac that opens from a slit at the junction of the middle and caudal third of the cervical trachea, and some penguins and petrels have double tracheas. The males of many waterfowl species have a tracheal bulbous expansion, and some birds, such as cranes ( Gruidae), have complex tracheal loops or coils that may be located in the caudal neck, within the keel, or within the thorax and keel (Fig. 1).

Figure 1. Examples of tracheal loops found in black swans ( Cygnus atratus), whooper swans (Cygnus cygnus), white spoonbills (Platalea leucorodia), helmeted curassows (Crax Pauxi), and whooping Cranes (Grus americana); adapted from [2]. To view click on figure The typical bird trachea is 2.7 times longer and 1.29 times wider than that of similarly sized mammals. The net effect is that tracheal resistance to air flow is similar to that in mammals, but the tracheal dead space volume is

about 4.5 times larger [2]. Birds compensate for the larger tracheal dead space by having a relatively larger tidal volume and a lower respiratory frequency, approximately one-third that of mammals. These two factors lessen the impact of the larger tracheal dead space volume on ventilation. Thus, minute tracheal ventilation is only about 1.5 to 1.9 times that of mammals. Implications for Anesthetic Management Because of the complete cartilaginous tracheal rings, an overly inflated endotracheal tube cuff can traumatize or rupture the tracheal mucosa and rings. For this reason, an endotracheal tube cuff either should not be inflated, or it should be inflated only sufficiently to form an effective seal when ventilation is assisted or controlled. Damage to the trachea may not become evident until as much as 5 to 7 days after intubation when the healing process and subsequent fibrotic narrowing of the tracheal lumen cause signs of dyspnea. The fully conscious, healthy, unmedicated bird obviously can compensate for the larger tracheal dead space. However, under the depressant effects of anesthetic drugs, ventilation is depressed and a greater percentage of minute ventilation becomes dead space ventilation. The consequence is that ventilation is less efficient in anesthetized birds. Intubating small birds has risks because endotracheal tubes with small internal diameters can impose significant resistance to air flow, especially if mucus accumulates in the tube. During anesthesia, mucus production can be copious and, with the drying effects of the inspired cold, dry gases, the mucus becomes thick and tenacious. Endotracheal tube obstruction can be detected by monitoring the bird's pattern of ventilation. As the airway becomes occluded, the duration of the expiratory phase becomes prolonged. Mechanically sighing the bird usually confirms the presence of an obstruction because the air sacs will fill in a relatively normal manner during inspiration, but will empty slowly or not at all during expiration. An anticholinergic, such as atropine or glycopyrrolate, reduces mucus production and decreases mucus plug formation, but may also increase mucus viscosity, making it harder to clear. Some avian practitioners avoid using anticholinergics in birds because these drugs increase heart rate, thus increasing the work of the heart and myocardial oxygen demand. These potentially adverse cardiac effects of anticholinergics must be weighed against their benefits. Air Sacs Birds have 9 air sacs, 4 paired and one unpaired. Depending upon the species, air sacs may have diverticula that enter and aerate the cervical vertebrae, some of the thoracic vertebrae, vertebral ribs, sternum, humerus, pelvis, and head and body of the femur. Air sacs, provide a tidal flow of air to the rigid avian lung, but do not contribute significantly to gas exchange.

Implications for Anesthesia It has been suggested that air sacs sequester or concentrate anesthetic gases and then, through some unknown mechanism, release the concentrated anesthetic gas to the lungs causing an anesthetic overdose and death of the hapless bird. For this scenario to have any validity, air sacs must possess two features: a blood-gas interface that enables the exchange of gases between air sacs and blood, and the ability to selectively concentrate inhalant anesthetics and not other gases. In fact, air sacs are avascular and there is no known biological tissue or mechanism that selectively concentrates inhalant anesthetics, rendering the above scenario unrealistic. Air sacs do not contribute significantly to gas exchange of either oxygen, carbon dioxide, or anesthetic gases. Body position of an anesthetized bird can significantly affect ventilation. During dorsal recumbency the weight of the abdominal viscera compresses the abdominal air sacs and reduces their effective volume, thus reducing ventilation. Gas Exchange Component Gas exchange occurs within the tertiary bronchi (parabronchi) and surrounding mantle of vascular rich tissue. The parabronchi are narrow tubes the inner surfaces of which are pierced by numerous openings into individual chambers called atria from which air capillaries extend. There are two types of parabronchial tissue in the avian lung. Paleopulmonic parabronchial tissue is found in all birds and consists of parallel, minimally anastomosing parabronchi. Neopulmonic parabronchial tissue is a meshwork of anastomosing parabronchi located in the caudolateral portion of each lung. The paleopulmonic and neopulmonic parabronchi are histologically indistinguishable from each other, but the direction of gas flow differs within the two types of lung. Gas flow in the paleopulmonic lung is unidirectional throughout the respiratory cycle while it is bi-directional in the neopulmonic parabronchi. The degree to which the neopulmonic lung is developed varies among species, being most highly developed in fowl and song birds in which it accounts for 20 to 25% of total lung volume. Penguins and emu have only paleopulmonic parabronchi, while pigeons, ducks, and cranes have both paleopulmonic and neopulmonic parabronchi with the neopulmonic lung accounting for 10 to 12% of total lung volume. Implications for Anesthetic Management During positive pressure ventilation it is possible that the direction of gas flow within the avian lung, especially the paleopulmonic lung, may be reversed. Fortunately this reversal of direction does not affect gas exchange because the gas exchange efficiency of the avian lung does not depend on the direction of flow [3].

The nature of the avian respiratory system makes it possible to ventilate birds with a continuous stream of an oxygen containing gas mixture introduced through the trachea and lungs and out through a ruptured or cannulated air sac. Alternatively, the gas mixture can be introduced through a cannula inserted into an air sac, across the lungs and out the trachea [4,5]. If the gas mixture also contains an inhalant anesthetic, then these techniques can be used to induce and maintain anesthesia in birds. Air sac cannulation is a technique that can be used to ventilate and resuscitate an apneic bird or a bird with an obstructed airway [6]. In a study comparing arterial blood gases from pentobarbital-anesthetized, spontaneously breathing ducks before and after cannulation of the clavicular air sac, PaO 2 and PaCO2 remained unchanged following air sac cannulation [7]. In other words, air sac cannulation did not impair ventilation or gas exchange. Mechanics of Ventilation Muscles of Respiration and the Thoracic Skeleton Birds do not possess a muscular diaphragm, but depend on cervical, thoracic and abdominal muscles for inspiration and expiration, both of which are active processes requiring muscular activity. During inspiration, the inspiratory muscles contract and the internal volume of the thoracoabdominal cavity increases (Fig. 2).

Figure 2. Changes in the position of the thoracic skeleton during breathing in a bird. The solid lines represent thoracic position at the end of expiration while the dotted lines show the thoracic position at the end of inspiration. From [31] with permission. To view click on figure Since the air sacs are the only significant volume-compliant structures within the body cavity, their volume also increases. As pressure within the air sacs becomes negative relative to ambient atmospheric pressure, air flows from the atmosphere into the pulmonary system. As a result of inspiratory valving (see below), during inspiration there is no or little flow in the ventrobronchi that connect the parabronchi and the intrapulmonary bronchus and, as a result, the inspired gas continues caudally through the intrapulmonary bronchus. A portion of the gas crosses the neopulmonic lung and continues into the caudal thoracic and abdominal air sacs, while an equal portion goes to the dorsobronchi and thence across the paleopulmonic lung (Fig. 3a and Fig. 3b).

Figure 3a. see legend below. To view click on figure

Figure 3b. see legend below. To view click on figure Figure 3a and 3b. Schematic representation of the right paleopulmonic lung and air sacs of a bird and the pathway of gas flow through the pulmonary system during inspiration and expiration. For purposes of clarity the neopulmonic lung is not shown. The intrapulmonary bronchus is also known as the mesobronchus. A - Inspiration. B - Expiration; adapted from [29,30]; by John Ludders and Michael Simmons, artist. During contraction of the expiratory muscles the internal volume of the thoracoabdominal cavity decreases, pressure within the air sacs increases, and gas flows out of the caudal thoracic and abdominal air sacs, passes across the neopulmonic lungs to the paleopulmonic lungs and thence out the ventrobronchi and trachea to the environment (Fig. 3a and Fig. 3b). Gas flow from the cranial air sacs does not pass back through the parabronchi but goes to the ventrobronchi, the trachea and thence to the environment. During expiration there is little or no flow in the intrapulmonary bronchus as a result of expiratory valving (see above). Direction of Gas Flow During inspiration and expiration the direction of gas flow in the paleopulmonic parabronchi is unidirectional, but in the neopulmonic parabronchi it is bi-directional. The unidirectional flow of gas through the intrapulmonary bronchus, the secondary bronchi, and the paleopulmonic parabronchi is governed by processes of aerodynamic valving and not by mechanical valving mechanisms such as valve leaflets or tissue dams. Aerodynamic valving occurs during both inspiration and expiration, but the controlling factors for each appear to vary. Inspiratory valving occurs primarily as a consequence of gas convective inertial forces (gas flow and density), and the accelerating effects of a constriction in the primary bronchus just cranial to where the ventrobronchi arise [8-10]. Additional factors involved in inspiratory valving include the orientation of secondary bronchial and air sac orifices in relationship to the direction of gas flow, and pressure differences between the cranial and caudal groups of air sacs. The net effect is that the inspired gas stream continues straight along the axis of the primary bronchus and intrapulmonary bronchus (mesobronchus) rather than turning into the ventrobronchi and the cranial air sacs. Expiratory valving, or that mechanism directing gas from the caudal thoracic and abdominal air sacs to and through the dorsobronchi and then the parabronchi, is not influenced by gas density, but is affected by dynamic compression of the intrapulmonary bronchus, a phenomenon that is affected by viscous resistance and gas flow [11]. Dynamic compression occurs when pressure in the air sacs is greater than the pressure in the lumen of the intrapulmonary bronchus. As a result of this pressure gradient

the bronchus tends to collapse to some degree. In addition, the greater the gas flow the greater will be the pressure exerted on the bronchus. In general, the efficiency of both inspiratory and expiratory valving decreases at low flows. Implications for Anesthetic Management Because both inspiration and expiration require muscle activity, anything that depresses muscle function, or impairs thoracic movement, will negatively affect ventilation. In general, anesthetic drugs cause muscle relaxation and the degree of relaxation depends on the anesthetic(s), depth of anesthesia, and physical condition of the bird. Control of Ventilation Ventilation and breathing pattern are regulated to meet the demands imposed by changes in metabolic activity (e.g., rest and flight) as well as other demands on the system imposed by a wide range of sensory inputs (e.g., heat and cold), forebrain controlled behavior, and emotional inputs. It must be kept in mind that birds do not have a diaphragm and as such do not have a phrenic nerve. It is assumed that there is a central respiratory control center in the avian brain, but this has not been unequivocally demonstrated. As in mammals, the central pattern generator appears to be located in the pons and medulla oblongata with facilitation and inhibition coming from higher regions of the brain. It also appears that the chemical drive on respiratory frequency and inspiratory and expiratory duration depend on vagal afferent feedback from receptors in the lung as well as on extrapulmonary chemoreceptors, mechanoreceptors, and thermoreceptors [12]. Chemoreceptors Central chemoreceptors affect ventilation in response to changes in arterial PCO2, and hydrogen ion concentration. Peripheral extrapulmonary chemoreceptors, specifically the carotid bodies, are influenced by PaO 2 and increase their discharge rate as PaO2 decreases, thus increasing ventilation; they transiently decrease their rate of discharge as PaO 2 increases, or when PaCO2 decreases. These responses are the same as those observed in mammals. Unlike mammals, birds have a unique group of peripheral receptors located in the lung called intrapulmonary chemoreceptors (IPC) that are acutely sensitive to carbon dioxide and insensitive to hypoxia. The IPC affect rate and volume of breathing on a breath-to-breath basis by acting as the afferent limb of an inspiratory-inhibitory reflex that is sensitive to the timing, rate, and extent of CO2 washout from the lung during inspiration. Implications for Anesthetic Management

Inhalant anesthetics, through their effects on the central nervous system and peripheral chemoreceptors, significantly depress ventilatory responses to hypoxia and hypercarbia in birds just as in mammals. More specifically, halothane has been shown to depress the responsiveness of IPC to CO 2 [13]. Thus, birds anesthetized with halothane are less able to adjust ventilation in response to changes in carbon dioxide levels. It is reasonable to assume that isoflurane has similar effects on IPC. Inhalant anesthetics typically are delivered in 100% oxygen. High fractions of inspired oxygen (FIO2) have been shown to depress ventilation probably through their effect on oxygen chemoreceptors [14]. At fractions of inspired oxygen greater than 40% ducks hypoventilated, but did not hypoventilate when FIO2 was closer to 21% (Table 1). Although both respiratory rate and tidal volume did not decrease significantly as FIO 2 increased, they tended to decrease and the cumulative effect resulted in hypoventilation. Interestingly the decrease in tidal volume correlated significantly with increasing PaCO 2, indicating that increasing FIO2 affects tidal volume more than respiratory frequency. This means that if respiratory frequency is used as an indicator of anesthetic depth or respiratory depression in the anesthetized bird, then the true condition of the bird is likely to be misinterpreted. Tidal volume is much more difficult to quantify in the anesthetized bird, but it is likely to be the better indicator of anesthetic depth and adequacy of ventilation. Table 1. Ventilatory and blood gas variables measured in spontaneously breathing ducks at four fractions of inspired oxygen (21%, 40%, 70%, and >90%) during constant (1.4%) end-tidal isoflurane anesthesia. Variable f (breaths/min) Vt (ml) Vmin (ml/min) pH PaCO2 (mm Hg) PaO2 (mm Hg) HCO3 (mEq/L) BB 21 % 6 82 528 7.42 33 85 20 -2 40 % 5 67 411 7.33 39 151 19 -5 70 % 4 77 394 7.31 42 278 18 -4.6 >90 % 6 82 384 7.33 42 369 19 -3.3

Data are median; ETiso = end-tidal isoflurane; Vt = tidal volume; Vmin = minute ventilation; PaCO2 = partial pressure of carbon dioxide in arterial

blood; PaO2 = partial pressure of oxygen in arterial blood; HCO 3 = bicarbonate; BB = base balance. [14] General Considerations for Anesthesia Physical Examination Every bird should be given a thorough physical examination prior to anesthesia. A number of excellent texts describe in detail the techniques for physical examination and what to look for in specific avian species [4,15,16]. In general, quietly observing a bird in its cage provides a great deal of information. Awareness of and attention to its surrounding environment, body form and posture, feather condition, and respiratory rate all provide clues to a bird's physical condition. Birds should be removed from their cage and examined, with particular attention given to the nares and mouth. A stethoscope with a pediatric head for small species should be used to examine the heart and lungs. At the same time the sharpness of the keel should be determined, as this is a good indicator of muscle mass and body condition. Acclimation When possible, a bird should be allowed to acclimate to the clinic or hospital environment prior to anesthesia. A bird brought into a new environment will be stressed. Time allows the bird to calm down after the initial physical examination and gives the veterinarian time to evaluate the results of blood work. It is not unusual that once a bird has acclimated to a new environment other disease signs, not obvious when the bird was first observed, may become apparent. Fasting Whether to fast birds prior to anesthesia and surgery is controversial. In general it has been recommended that birds either not be fasted or be fasted for no more than 2 to 3 hours prior to anesthesia because of their high metabolic rate, poor hepatic glycogen storage and, thus, the possibility of developing hypoglycemia during anesthesia. However, regurgitation in birds and the subsequent airway obstruction that can occur in birds that have not been fasted is possible. As a result some practitioners recommend that avian species, regardless of size, be fasted overnight. My experience with waterfowl, cranes, and ratites also suggests that an overnight fast reduces the incidence of regurgitation-associated problems and is not deleterious to a bird as long as it is not in a negative metabolic balance, which may predispose it to developing hypoglycemia. Premedicants such as tranquilizers, sedatives and analgesics, are frequently used in the anesthetic management of birds and they reduce the amount of inhalant anesthetic needed to maintain anesthesia. In cockatoos ( Cacatua spp.), butorphanol (1 mg/kg, IM) has been shown to decrease the minimum alveolar concentration (MAC) of isoflurane by 25% [17]. In a study in

chickens [18], morphine (0.1, 1.0, 3.0 mg/kg, IV) reduced isoflurane MAC by 15, 39, and 52% while the kappa opioid agonist U504488H at the same doses reduced MAC by 13, 27 and 39%. Midazolam is frequently used to produce anxiolysis in birds and facilitate physical restraint and induction of general inhalant anesthesia. Although there are no studies investigating the MAC sparing effect of this drug in birds, my clinical impression is that it can significantly reduce the amount of inhalant anesthetic needed to maintain anesthesia. In practice this means that after a short period of time during which the bird equilibrates with the isoflurane, the vaporizer dial setting is less than 1.5% and often it is closer to 1.0%. The key point is that these premedicants significantly reduce the amount of inhalant anesthetic needed to maintain anesthesia and by so doing they reduce the amount of cardiovascular depression typically associated with high concentrations of inhalant anesthetics. Inhalational Anesthesia Inhalant anesthetics, compared to injectable anesthetics, offer several advantages for patient management, including rapid induction and recovery, especially when inhalant anesthetics of low blood/gas solubility are used (isoflurane and sevoflurane), easier control of anesthetic depth, the improved oxygenation due to the concurrent use of oxygen, and recovery that is not dependent on metabolic or excretory pathways that may be altered or impaired in the diseased bird. There are some disadvantages, of course, including the requirement for special equipment such as a source of oxygen, a vaporizer, breathing circuit, and a mechanism for scavenging waste anesthetic gases. Breathing Circuits Non-rebreathing circuits, such as the Bain circuit or Norman elbow, are ideal for use in birds weighing less than 7 kg because they offer minimal resistance to patient ventilation. Anything that reduces the work of breathing in anesthetized birds will lessen the negative effects of anesthesia on ventilation. A reasonable fresh gas flow rate for the Bain circuit is 150 - 200 ml/kg/min with flows no lower than 500 ml/min. Standard circle systems can be used for larger birds and large animal circuits have been used in ratites. MAC The minimum alveolar concentration that produces anesthesia in mammals exposed to a noxious stimulus is referred to as MAC. It is a measure that makes it possible to compare concentration and effect among inhalant anesthetics. Strictly speaking the term is not appropriate for birds as they do not have an alveolar lung. A better term and definition when discussing the use of inhalant anesthetics in birds, as long as the methods for determining MAC are similar to those used in mammals, is the minimum anesthetic concentration needed to produce anesthesia. The MAC values for

halothane, isoflurane and sevoflurane in birds (Table 2) are similar to MAC values reported for mammals [19-23]. Table 2. Minimum anesthetic concentrations (MAC) for halothane, isoflurane and sevoflurane in selected avian species. Birds Cockatoo Chicken Ducks Sandhill Cranes Halothane(%) 0.85 [19] 1.05 [22] Isoflurane (%) 1.44 [17] 1.32 [21] 1.35 [20] Sevoflurane (%) 2.21 [23] -

Halothane, isoflurane and sevoflurane depress ventilation at all end-tidal anesthetic concentrations and in a dose-dependent manner [19-23], and they appear to do so much more in birds than in mammals as indicated by anesthetic index (AI), a measure of the tendency for an inhalant anesthetic to cause respiratory depression to the point of apnea. The smaller the AI value for an inhalant the greater is its ventilatory depression. In ducks, AI is 1.51 for halothane [22] and 1.65 for isoflurane [21], values that are lower than those reported for the same anesthetics in dogs, cats, and horses. In view of the many anesthetic-related factors that directly or indirectly depress ventilation in birds, it is not surprising that they hypoventilate to a greater degree than do mammals under comparable anesthetic conditions. When a bird hypoventilates during general inhalational anesthesia not only is it difficult to control the plane of anesthesia, but the attendant hypercapnia can have adverse effects on cardiac function. In a study of 12 ducks anesthetized with halothane (1.5%) and that inspired several fractions of CO2, unifocal and multifocal premature ventricular contractions developed in 6 ducks at a mean PaCO2 of 67 +12 mmHg [24]. When inhalation of CO2 was discontinued, the arrhythmias ceased in 5 of the 6 ducks. When possible it is reasonable to assist or control ventilation during general inhalant anesthesia of birds. The effect of halothane on blood pressure can be variable. In chickens and ducks, increasing concentrations of halothane cause a decrease in mean arterial blood pressure [19,25,26], or no change [22]. In contrast, isoflurane appears to consistently cause a dose-dependent decrease in mean arterial blood pressure, [20,21,25,26] which may be due to the fact that isoflurane consistently causes peripheral vasodilatation. Sevoflurane, on the other hand, dose-dependently decreases blood pressure during controlled ventilation, but not during spontaneous ventilation [Personal communication from Naganobu K, Miyazaki University, Miyazaki, Japan; January 2001], the latter phenomenon is probably due to hypercarbia-induced increases in sympathetic tone which causes hypertension.

In mammals, positive pressure ventilation depresses mean arterial blood pressure by creating positive intrathoracic pressures that compress the great vessels and impede the venous return of blood to the heart. In Sandhill cranes anesthetized with isoflurane, mean arterial blood pressure was actually higher during positive pressure ventilation than during spontaneous ventilation [20]. This was not the case in chickens anesthetized with sevoflurane in which mean blood pressure was lower during positive pressure ventilation than during spontaneous ventilation [Personal communication from Naganobu K, Miyazaki University, Miyazaki, Japan; January 2001]. Cardiac arrhythmias frequently occur in birds anesthetized with halothane. Cardiac stability is one of the perceived advantages of isoflurane and is one of the reasons why it has so readily gained wide acceptance in clinical avian practice. However, in a study in which an electrical fibrillation model was used to investigate the myocardial irritant effects of isoflurane and halothane, isoflurane was found to lower the threshold for electrical fibrillation more so than halothane [26]. The reason(s) for the discrepancy between clinical experience and this research model is not clear. Cardiac arrhythmias do occur during isoflurane anesthesia in birds, but they are not as severe or as life threatening as are those associated with halothane anesthesia. Chickens anesthetized with sevoflurane did not have any evidence of cardiac arrhythmias during anesthesia [23]. Nitrous oxide can be used as an adjunct to general anesthesia in birds, but must not be used as the sole anesthetic. Nitrous oxide is not sequestered in or concentrated by air sacs, and considerations for its use are similar to those for mammals. Respiratory function should be normal and adequate oxygen should be provided to meet the metabolic demands of the patient. This means that a minimum of 30% oxygen should be provided in the anesthetic gas mixture. Some birds may have unique anatomic features that preclude the use of nitrous oxide. For example, pelicans have subcutaneous pockets of air that do not communicate with the respiratory system and, as a result, nitrous oxide administered to these birds can cause subcutaneous emphysema [27]. Once the nitrous oxide is discontinued this condition is reversible, but possible complications can be avoided in these birds by omitting nitrous oxide from the anesthetic plan. Muscle Paralytics as Adjuncts to General Inhalational Anesthesia Muscle paralytics may be useful adjuncts for the anesthetic management of birds, especially during long surgical procedures requiring a greater degree of muscular relaxation and immobility than that provided by anesthetic drugs alone. Because muscle paralytics cause skeletal muscle paralysis and do not provide any analgesia, it is incumbent on the anesthetist to control breathing with positive pressure ventilation, and to provide sufficient analgesia/anesthesia so that the bird does not experience pain.

Atracurium is a non-depolarizing muscle relaxant with short duration of effect and minimal cardiovascular effects. The effective dose associated with 95% twitch depression in 12 of 24 chickens (ED95/50) was 0.25 mg/kg, IV, and ED95/95 was 0.46 mg/kg, IV [28]. The duration of action for the lower dose was 34.5 5.8 minutes, and 47.8 10.3 minutes at the higher dose. Edrophonium (0.5 mg/kg, IV) reversed the effects of atracurium. There were small but statistically significant changes in cardiovascular variables in that heart rate decreased and blood pressure increased after administration of atracurium, but these changes were considered to be clinically unimportant. References

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Click on the author's name to view a list of his/her publications: J. W. Ludders All rights reserved. This document is available on-line at www.ivis.org. Document No. A1410.0301