(PDF) Respiratory diseases and their effects on respiratory function and exercise capacity

bs_bs_banner Equine Veterinary Journal ISSN 0425-1644 DOI: 10.1111/evj.12028 Review Article Respiratory diseases and their effects on respiratory function and exercise capacity E. VAN ERCK-WESTERGREN†, S. H. FRANKLIN‡ and W. M. BAYLY*§ † Equine Sports Medicine Practice, Waterloo, Belgium School of Animal and Veterinary Sciences, University of Adelaide, South Australia, Australia § Ofﬁce of the Provost, Washington State University, USA. ‡ *Correspondence email: wmb@wsu.edu; Received: 14.03.11; Accepted: 02.12.12 Summary Given that aerobic metabolism is the predominant energy pathway for most sports, the respiratory system can be a rate-limiting factor in the exercise capacity of ﬁt and healthy horses. Consequently, respiratory diseases, even in mild forms, are potentially deleterious to any athletic performance. The functional impairment associated with a respiratory condition depends on the degree of severity of the disease and the equestrian discipline involved. Respiratory abnormalities generally result in an increase in respiratory impedance and work of breathing and a reduced level of ventilation that can be detected objectively by deterioration in breathing mechanics and arterial blood gas tensions and/or lactataemia. The overall prevalence of airway diseases is comparatively high in equine athletes and may affect the upper airways, lower airways or both. Diseases of the airways have been associated with a wide variety of anatomical and/or inﬂammatory conditions. In some instances, the diagnosis is challenging because conditions can be subclinical in horses at rest and become clinically relevant only during exercise. In such cases, an exercise test may be warranted in the evaluation of the patient. The design of the exercise test is critical to inducing the clinical signs of the problem and establishing an accurate diagnosis. Additional diagnostic techniques, such as airway sampling, can be valuable in the diagnosis of subclinical lower airway problems that have the capacity to impair performance. As all these techniques become more widely used in practice, they should inevitably enhance veterinarians’ diagnostic capabilities and improve their assessment of treatment effectiveness and the long-term management of equine athletes. Keywords: horse; respiratory disease; lower airways; upper airways; respiratory function; exercise Introduction Healthy trained horses commonly experience hypoxaemia and hypercapnia during strenuous exercise. The causes and consequences of these ﬁndings are described in detail elsewhere [1]. As a consequence, the occurrence of any respiratory disease, even mild in nature, has the potential to impair gas exchange further through diffusion or ventilation limitation and subsequently cause decreased performance. Certainly, respiratory diseases have been identiﬁed as an important cause of poor performance in athletic horses [2–5]. The impact of respiratory disease will depend not only on the nature and severity of the disease but also on the equestrian discipline performed. In horses competing at maximal and supramaximal intensities, maximal efﬁciency of all body systems, including the respiratory system, is essential. Respiratory disease in racehorses will impair their performances more markedly than those of horses exercising at less strenuous levels, such as dressage horses or showjumpers. The oxygen consumption associated with the dressage or showjumping is less, as is the work of breathing [6], and a smaller fraction of their total respiratory capacity is required. Respiratory disease is common in equine athletes and may affect the upper airways, lower airways or both. The prevalence of lower airway diseases is high in equine athletes, with reports ranging from 20% in adult horses to 80% in young Thoroughbreds in training [7–10]. A high prevalence (>50%) is encountered in horses working in all equestrian disciplines, from racing Standardbreds [4,11] to endurance horses [5] and pleasure horses [12–14]. Nevertheless, this prevalence may easily be underestimated, because most conditions progress subclinically, and relevant diagnostic procedures are sometimes difﬁcult to implement routinely in the ﬁeld. The high prevalence of lower airway diseases in the equine population may be attributed to several well-identiﬁed factors related to their work and environment [8,15,16]. The true prevalence of upper airway disorders is difﬁcult to ascertain. Many conditions are dynamic in nature, hence they are not necessarily evident during a resting examination [17–20]. Nevertheless, both treadmill and overground endoscopy studies have revealed that upper respiratory tract (URT) collapse is an important cause of poor performance, both in racehorses [2,19,21–24] and in other sport horses [25–27]. Furthermore, 376 horses with URT collapse frequently have concurrent lower airway disease [11,28,29]. Upper airway disorders and their effects on respiratory function and exercise capacity Diagnosis of dynamic upper respiratory tract disorders during exercise Videoendoscopy during exercise is considered to be the ‘gold standard’ for making a deﬁnitive diagnosis of dynamic upper airway collapse in horses, where resting ﬁndings are frequently unreliable or absent [3,19,21,22,30,31]. Although the grading of laryngeal function at rest can help to predict the degree of laryngeal obstruction observed during exercise [32], cases relating to palatal instability, dorsal displacement of the soft palate or pharyngeal collapse do not correlate with resting observations [19,27,33]. Exercising endoscopy has traditionally been performed within a laboratory environment whereby horses are examined during exercise on a high-speed treadmill. This technique has greatly aided our understanding of the different forms of dynamic airway collapse that may affect exercising horses and has been used both for clinical investigations and for research purposes. The misperception that treadmills are unsafe [34] and the necessity to evaluate horses in ridden conditions has warranted the development of overground videoendoscopy [35]. Recent advances in technology have enabled the development of portable endoscopes that may be used during ridden or driven exercise in the ﬁeld (Fig 1) [23,24,35–37]. The advantages of overground endoscopy include the ability to exercise the horse in its natural environment while being ridden and without the need for referral to a specialist centre with a treadmill. This is less time consuming and also has the potential beneﬁt of examining the horse in conditions similar to those experienced during usual work or competition [38]. Previously, it has been suggested that because treadmill exercise does not entirely replicate ﬁeld exercise conditions; this may lead to some conditions being underdiagnosed [27]. Equine Veterinary Journal 45 (2013) 376–387 © 2013 EVJ Ltd E. Van Erck-Westergren et al. Fig 1: The ability to stabilise the position of an endoscope (arrowed) and to record its ﬁbreoptic images digitally as the horse exercises over ground represents a new dimension in the investigation of upper airway respiratory noise and/or obstruction. It is important to note that whilst videoendoscopy enables visualisation of any dynamic airway collapse, it does not enable quantiﬁcation of the functional effects of an obstruction. It has therefore been suggested that to assess any respiratory limitation deﬁnitively, it is necessary to measure upper airway mechanics [39]. However, this is not commonly performed in clinical practice. Factors predisposing to equine upper respiratory tract disorders Horses are particularly prone to developing dynamic upper airway collapse because they are obligatory nasal breathers and cannot avoid the high pressures associated with nasal breathing as can other species that switch to oral breathing during exercise [40,41]. The equine upper airways are highly collapsible, especially in the nasopharyngeal region, which is not supported by osseous or cartilagenous structures. The nasopharynx relies solely on local muscular activity to maintain stability and patency. The palatal muscles, extrinsic tongue muscles, hyoid muscles and pharyngeal dilator muscles have demonstrated a level of respiratory-dependent activity, determined by the amplitude of airﬂow and pressure variations [42–45]. During exercise, upper airway muscular activity is triggered by pressure-sensing mechanoreceptors and chemoreceptors in the pharynx and larynx, which detect changes in pressure, mechanical deformation, increased levels of carbon dioxide and changes in temperature [46,47]. The dramatic variations in airway ﬂow and transmural pressures that are encountered during intense exertion promote instability and potential secondary dynamic obstruction of the upper airways. Based on a simulated model of normal equine upper airways, Rakesh et al. [48] showed that during inhalation the most negative pressures and highest airﬂow turbulence occur at the ﬂoor of the rostral aspect of the nasopharynx and within the larynx. It is perhaps not surprising, therefore, to ﬁnd that these are the areas where dynamic airway collapse occurs most commonly. Not all upper airway obstructive conditions have the same impact on respiratory function, but they commonly create an increase in respiratory resistance along the URT, which may result in either reduced airﬂow or an increase in the trans-upper airway pressures required to maintain airﬂow [49,50]. This increase in airway resistance will lead to an increase in respiratory workload, and where airﬂow is reduced the resulting hypoventilation may lead to decreased oxygen consumption, increased blood lactate concentration and exacerbation of arterial hypoxaemia and hypercapnia. A number of factors are implicated in the development of dynamic upper respiratory tract collapse in an individual horse. In many cases, the presence and severity of this and the associated narrowing of the airway are linked to the type of exercise and its intensity, with many forms of URT collapse only occurring during strenuous work. This is not surprising given Equine Veterinary Journal 45 (2013) 376–387 © 2013 EVJ Ltd Responses of horses with respiratory disease to exercise the fact that transpulmonary inspiratory pressures become more negative as speed increases [51–53]. Fatigue of the respiratory musculature may also play a role. Hence, the type of exercise test performed will have an impact on the ability to make a deﬁnitive diagnosis of dynamic URT collapse [54]. In particular, when investigating horses that are reported to experience exercise intolerance and abnormal respiratory noise only during competition, it is necessary to recreate the work effort encountered in those circumstances. Allen and Franklin [54] found that dorsal displacement of the soft palate (DDSP) was more likely to be observed in horses that undertook longer exercise tests and that tests on a circular gallop or track were preferable to those performed in intervals on short gallops. Other equitation factors, including poll ﬂexion and factors relating to the bit and bridle, may also be implicated in the development of dynamic URT collapse [27,55]. These factors are particularly important in pleasure or sport horses, where dynamic airway collapse appears commonly to occur at lower exercise intensities than in racehorses. Van Erck et al. [36] found that pharyngeal collapse was more readily diagnosed in pleasure horses during overground endoscopy compared with treadmill endoscopy. This is likely to be due to the fact that riding factors, including increased tension in the reins and head ﬂexion, are frequently an important predisposing factor in the development of dynamic airway collapse in these horses [25–27,55]. Changes in poll ﬂexion are easier to create during ridden exercise, although it is possible to induce these during treadmill exercise [25,56,57]. Changes in head and neck position have a signiﬁcant effect on pharyngeal diameter, with the smallest diameter being found when in a dorsal ﬂexed position [58]. Correspondingly, increased poll ﬂexion leads to an increase in respiratory resistance and inspiratory pressures and results in decreased inspiratory ﬂows [56]. In addition, the ﬂexed position increases the compliance of the upper airway walls and promotes the bulging of soft tissues within the upper airways [56,59]. Upper airway instability is markedly affected by equitation and rider interaction (Fig 2). In a recent study looking at the effects of riding and head ﬂexion on upper airway function, 90 and 81% of the horses developed or showed an aggravation in the severity of upper airway obstructive disorders with head ﬂexion and rider intervention, respectively [27]. In dressage horses, usually worked with a more acute head–neck angle, head ﬂexion and riding had a more signiﬁcant inﬂuence on the development of upper airway obstruction than in showjumpers, and rider intervention and exercising with increased head ﬂexion increased the detection of all dynamic upper airway obstructive conditions, except DDSP. Priest et al. [38] recently reported a case of DDSP in a racing Standardbred that occurred in association with the driver grabbing a strong hold of the lines. Fig 2: Ridden warmblood equipped with an overground endoscopea. Upper airway stability is inﬂuenced by poll ﬂexion and equitation manoeuvres. The possibility of investigating upper airway mechanics during ridden exercise or in conditions similar to normal exercise is important to achieve an accurate diagnosis. 377 E. Van Erck-Westergren et al. Responses of horses with respiratory disease to exercise a) b) Fig 3: Upper airway endoscopy in a dressage horse referred for exercise intolerance. a) Dorsoventral pharyngeal collapse and palatal instability, resulting in almost complete obstruction, was observed when the horse was placed with his poll ﬂexed and tension placed on the reins. b) No abnormality occurred when the horse was exercised with his head in extension. Recurrent laryngeal neuropathy Recurrent laryngeal neuropathy (RLN or idiopathic laryngeal hemiplegia), has long been identiﬁed as a major cause of poor performance [60] and is the condition that has been most studied with respect to its effect on respiratory function and exercise capacity. The condition has a signiﬁcant impact on respiratory function during exercise. Laryngeal function can be assessed through resting endoscopy, yet endoscopy during exercise is warranted in cases with some residual arytenoid function because the grade assigned during resting assessment does not necessarily predict the degree of laryngeal dysfunction and obstruction during strenuous exertion [17–20]. More recently, the use of laryngeal ultrasonography has been described as an adjunctive tool for diagnosis of RLN [61]. This technique has been found to be extremely accurate in predicting arytenoid dysfunction during exercise, with a sensitivity of 90% and speciﬁcity of 98% compared with resting endoscopy (sensitivity of 80% and speciﬁcity of 81%) [62]. Laryngeal ultrasonography is therefore considered to be a useful diagnostic modality for assessment of arytenoid function in horses with equivocal resting ﬁndings, especially where exercising endoscopy is unavailable. The dysfunction of the cricoarytenoidus dorsalis muscle due to RLN prevents complete abduction of the corresponding arytenoid cartilage and, according to its grade of severity, results in increased respiratory impedance that is measurable both at rest [63,64] and during exercise [65,66]. In strenuously exercising horses, RLN causes a more severe hypercapnic hypoxaemia, acidosis and a signiﬁcant reduction in peak oxygen consumption in comparison to horses with normal upper airway function [18,67–70]. Recurrent laryngeal neuropathy also reduces athletic capacity, as demonstrated by the decrease in speed at a heart rate of 200 beats/min [70]. A number of surgical treatments for RLN have been described, including prosthetic laryngoplasty, ventriculectomy, ventriculocordectomy, laser ventriculectomy, partial, total and subtotal arytenoidectomy, laryngeal reinnervation and electrical pacing of laryngeal muscles. Prosthetic laryngoplasty (ﬁrst described by Marks et al. [71]) currently remains the treatment of choice for athletic horses where airway obstruction and exercise intolerance are the primary concern [72]. Several experimental studies have shown that upper airway ﬂow mechanics are returned to baseline during submaximal exercise [65,73] and at exercise intensities that elicit maximal heart rate [74]. However, Radcliffe et al. [66] found that although ventilation was restored in experimental horses exercising at low velocity, this did not occur at the velocity eliciting maximal heart rate. Furthermore, blood gases during exercise were not returned to normal levels, which was consistent with the previously reported ﬁndings of Tate et al. [69]. Other procedures, such as ventriculectomy and arytenoidectomy, also do not entirely eliminate airway obstruction and are considered less effective than laryngoplasty at restoring airway patency [66,73,75,76]. The nerve–muscle pedicle graft technique is reported to be effective in restoring upper airway ﬂow mechanics in horses with experimentally induced laryngeal hemiplegia, although this may take up to a year to achieve [77]. Other studies to investigate the potential use of laryngeal pacemakers as an alternative treatment are ongoing [78,79]. Tolerance for upper airway obstruction depends on the type and level of equestrian discipline performed. Success rates for laryngoplasty are in the 378 region of 90% for horses performing submaximal exercise [80]; however, success rates for racehorses are substantially lower, ranging from about 60 [81–83] to 78% in National Hunt horses [84]. It has been proposed that stability of the arytenoid cartilage is more important than grade of abduction [65,85] and that full arytenoid abduction is not necessary to restore normal patency because the cross-sectional area of the trachea area is smaller than the rima glottidis [50]. Indeed, Barakzai et al. [85] found no difference in performance between horses with grade 1, 2 or 3 laryngeal function post laryngoplasty. Rakesh et al. [50] modelled the effects of different degrees of arytenoid abduction and found that a 25% decrease in cross-sectional area (grade 3) resulted in a 5.6% reduction of peak airﬂow and tidal volume. This was considered unlikely to be of signiﬁcance in horses other than racehorses. However, compared with full abduction and grade 2 abduction (12% decrease in cross-sectional area), the larynx itself was subjected to greater turbulence and more negative collapsing pressures, especially at its lateral and ventral aspects. This may predispose these horses to other forms of dynamic collapse, including collapse of the right vocal fold and axial deviation of the aryepiglottal folds. Indeed, 2 recent studies found that horses which present with abnormal respiratory noise following laryngoplasty may be afﬂicted with collapse of various structures within the URT, and URT collapse in these horses is frequently multifactorial [86,87]. Another possible reason for failure to restore athletic performance in some horses following surgical treatment of RLN is the presence of lower airway disease subsequent to tracheal aspiration following laryngoplasty, due to interference with the normal protective mechanism of the larynx [66,88]. Nasopharyngeal collapse A number of forms of nasopharyngeal collapse are described in exercising horses. Most common is DDSP [2,3,19,21], which is observed most commonly in racehorses and other horses undergoing strenuous exercise. Palatal instability is also observed frequently and is thought to be a precursor to DDSP [19,89]. Other forms of nasopharyngeal collapse may affect the walls, roof and/or ﬂoor of the nasopharynx [33]. Pharyngeal collapse occurs more commonly in sport horses, where it appears to be exacerbated by increased poll ﬂexion [25–27] (Fig 3). The pathophysiology of DDSP and of other forms of nasopharyngeal collapse, although not fully elucidated, is generally believed to involve common neuromuscular dysfunction of the upper airways [89]. However, it has proved difﬁcult to determine the precise involvement of the various elements of the complex anatomical relation between the intrinsic and extrinsic pharyngeal muscles, hyoid apparatus, larynx and muscles of the tongue. In DDSP, there is some evidence that neuromuscular dysfunction of the intrinsic palatal musculature, speciﬁcally the palatinus and palatopharyngeus muscles, plays an important role. Temporary blockade of the pharyngeal branch of the vagus that provides motor supply to these muscles has been shown to result in persistent DDSP at rest and during exercise [90]. Furthermore, histological abnormalities consistent with chronic denervation (ﬁbre type grouping, mild atrophy, moth-eaten ﬁbres and target ﬁbres) have been identiﬁed within the palatinus muscle in horses with conﬁrmed DDSP [45]. Inﬂammatory conditions, such as guttural pouch or pharyngeal lymphoid hyperplasia, could result in nasopharyngeal Equine Veterinary Journal 45 (2013) 376–387 © 2013 EVJ Ltd E. Van Erck-Westergren et al. instability and DDSP [47,91,92]. However, to date, no such causal relation has been found. Other studies have implicated extrinsic factors affecting laryngohyoid position as playing an important role in the development of DDSP. Early studies suggested that the ‘strap’ muscles (sternohyoideus, sternothyroideus and omohyoideus) attaching to the hyoid apparatus might result in laryngopalatal dislocation as a result of caudal retraction of the larynx [93]. The thyrohyoid muscles also affect the positioning of the hyoid apparatus and larynx [94]. Bilateral resection of these muscles was found to result in DDSP at slow-speed exercise in 7 of 10 horses and led to the development of the ‘tie-forward’ procedure as a treatment for DDSP [95]. More recently, muscles associated with the tongue have been implicated. Bilateral blockade of the hypoglossal nerve at the level of the ceratohyoid has been shown to result in nasopharyngeal instability and subsequent DDSP during high-speed exercise [96]. In other species also there is evidence that these muscles have respiratory-related activity and that electrical stimulation of the hypoglossal nerve increases upper airway dilatation [97,98]. In man, the genioglossus is considered to be the primary upper airway dilator muscle [99]. Dilatation and stabilisation of the dorsal and lateral walls of the nasopharynx are achieved by contraction of the stylopharyngeus muscle [100] and the pharyngeal constrictor muscles [101]. The stylopharyngeus muscle is the major dilator of the dorsal nasopharynx. Motor function is provided by the glossopharyngeal nerve, and bilateral blockade of this nerve has been shown to produce dorsal nasopharyngeal wall collapse in horses [100]. The pharyngeal constrictor muscles include the superior (dorsal) pharyngeal constrictor (composed of the palatopharyngeus and pterygopharyngeus muscles), the middle pharyngeal constrictor (hyopharyngeus) and the inferior pharyngeal constrictor (thyropharyngeus) [94,101]. These muscles are innervated by branches of the vagus nerve. They have a dual role in deglutition and respiration. Tonic activity of these muscles during respiration aids dilatation of the pharyngeal walls [101]. It is possible that dysfunction of one or more of these muscles may be implicated in dynamic pharyngeal wall collapse. Irrespective of the underlying cause, DDSP induces signiﬁcant alterations in upper airway pressures, a decrease in airﬂow and an increase in expiratory resistance in the upper airways [90,102,103]. In Thoroughbred racehorses referred for investigation of poor performance, DDSP resulted in a signiﬁcant reduction in minute ventilation and tidal volume but did not alter breathing frequency. The accompanying decrease of oxygen consumption was identiﬁed as the main cause of athletic impairment [103]. In cases with palatal instability, it is also likely that respiratory function and exercise capacity may be impaired in horses undergoing strenuous exercise, although this is not as severe as the limitations induced by DDSP [89]. In Warmblood showjumpers or dressage horses, nasopharyngeal instability has been associated with a decrease in performance [27]. Although the effects on airﬂow have not been reported for other forms of pharyngeal collapse, this disorder has been reported to be most commonly associated with blood gas abnormalities, when occurring either in isolation or in combination with other forms of URT collapse [104]. Pharyngeal lymphoid hyperplasia Pharyngeal lymphoid hyperplasia does not represent a primary disorder per se but rather, it is an inﬂammatory reaction secondary to immunological stimulation, which is usually physiological in young horses up to the age of 3 years [105]. Its effect on performance is still open to question. As an isolated condition, it has not been shown to alter upper airway function signiﬁcantly unless present in a severe form or associated with other respiratory problems [106–108]; however, recent epidemiological data indicate that mild to moderate degrees of lymphoid hyperplasia in the pharynx are negatively correlated to performances in racing Thoroughbreds [109]. The discrepancy in data regarding the effect of pharyngeal lymphoid hyperplasia may be due to differences in the populations studied (e.g. age, level of competition, occurrence of concomitant lower airway disease) [11]. Other upper airway disorders Other conditions occurring only during exercise, such as axial deviation of aryepiglottic folds, bilateral vocal fold collapse, epiglottal entrapment and Equine Veterinary Journal 45 (2013) 376–387 © 2013 EVJ Ltd Responses of horses with respiratory disease to exercise epiglottal retroversion, have also been associated with poor performance [3,19,25,27,44,70,110,111]; however, data regarding mechanical or metabolic consequences have not been documented. Complex obstructions, where more than one structure collapses into the airway, or combinations of upper and lower airway disorders occur frequently [3,4,19,22,27,112,113]. Multiple abnormalities will be associated more commonly with signiﬁcant gas exchange impairment than single disorders [11,28,112,114]. Lower airway disorders and their effects on respiratory function and exercise capacity Recurrent airway obstruction One of the most extensively studied equine respiratory diseases is recurrent airway obstruction (RAO). Also known as ‘heaves,’ RAO is a reversible lower airway disease affecting adult horses. While having a number of possible aetiologies, RAO is most commonly triggered by the inhalation of microscopic organic dust and moulds naturally present in the horse’s environment. It is considered to be a hypersensitivity reaction that results in neutrophilic inﬂammation in the lung and lower airways after an initial challenge [115]. The typical pathophysiological features of RAO resulting in airway obstruction are the accumulation and thickening of mucus in the airways, peribronchial oedema and reversible bronchospasm [116]. Even in the absence of speciﬁc moulds, horses may be hyperreactive to nonspeciﬁc stimuli, and an exacerbation of their symptoms may occur with inhalation of dust particles, airborne allergens and cold air. With proper environmental management, periods of clinical remission may be attained. Clinical manifestations of RAO are sometimes nonspeciﬁc and may vary in intensity and nature, depending on the stage (remission vs. crisis) and chronicity of the disease. These usually include cough, prolongation of the abdominal expiratory phase and increased breathing effort, accumulation of mucus in the tracheobronchial tree and decreased exercise tolerance [116]. The impact of RAO on performance has been recognised for a very long time. In athletic horses, the underlying pathophysiological processes leading to impaired performance have been partly elucidated by studying respiratory mechanics during rest and exercise. During a phase of exacerbation of the disease, signiﬁcant functional changes occur, such as an increase in maximal transpulmonary pressures, respiratory resistance and work of breathing, a decrease in dynamic lung compliance and arterial hypoxaemia [117–122]. Marked ventilation–perfusion mismatching has also been demonstrated and identiﬁed as a major cause of arterial hypoxaemia [123,124]. Heaves-affected horses also have an increased end-expiratory lung volume or functional residual capacity secondary to air trapped behind obstructed sections of airways [123]. The air-trapping phenomenon contributes to exacerbation of ventilation–perfusion inequalities and dead-space ventilation [125]. During submaximal exercise, RAO-affected horses show a decrease in expired minute ﬂow and an increase in work of breathing associated with hypoxaemia and hypercapnia, which contribute to aggravation of exercise-induced hypoventilation and cause premature hypoxaemia and lactate accumulation [126]. These factors are the source of the exercise intolerance during an acute episode of RAO. Another feature of RAO is airway hyperresponsiveness, which may impair performance in affected horses, even when they are in a remission phase of the disease. Hyperresponsiveness is manifest as bronchoconstriction in response to nonspeciﬁc stimuli (inhalation of cold air, noxious gases, dust particles and other irritants). In older horses with RAO, chronic remodelling of the airway structures may occur, further exacerbating dysfunction. Hypertrophy of peribronchial musculature and irreversible bronchiectasis have been described [127]. Recurrent airway obstruction-induced pathogenic changes are not only limited to the respiratory system. Secondary functional adaptations of the cardiovascular system have also been observed in association with RAO, such as an increase in resting pulmonary arterial pressure (PAP) [125,128] and transient morphological changes equivalent to cor pulmonale [129,130]. There is also evidence of structural changes in the skeletal muscles of heaves-affected horses when compared with 379 Responses of horses with respiratory disease to exercise those of healthy horses, and these may contribute to poor performance [131]. Inﬂammatory airway disease Inﬂammatory airway disease (IAD) has recently been deﬁned in an American College of Veterinary Internal Medicine Consensus Statement [132]. It was previously termed ‘mild bronchitis’ or ‘bronchiolitis’ in earlier papers to differentiate it from RAO [133,134]. Inﬂammatory airway disease is a nonseptic inﬂammatory condition, the diagnosis of which is based on evidence of increased inﬂammatory cells in the bronchoalveolar lavage ﬂuid (BALF) or ‘pulmonary dysfunction based on evidence of lower airway obstruction, airway hyperresponsiveness, or impaired blood gas exchange at rest or during exercise’. Coughing and excess tracheal mucus may be present irregularly, but increased respiratory effort at rest is not apparent. By deﬁnition, the condition is also a potential cause of poor performance, and it may be clinically indistinguishable from RAO. However, until new evidence regarding its functional consequences was recently produced, the impact of subclinical lower airway disease on performance was questioned. It was argued that this condition, like exercise-induced pulmonary haemorrhage (EIPH), was so common in racehorses and sport horses that its impact during exercise must be limited. Numerous epidemiological and experimental protocols have now shown that, although these conditions may not prevent horses from working or competing, they clearly generate respiratory dysfunction and may impede a horse’s performance. Inﬂammatory airway disease is highly prevalent in the racehorse population [2–4,10,135] and was identiﬁed as the second most common cause of wastage in young Thoroughbreds [10]. Based on racing statistics, MacNamara et al. [136] showed that Standardbreds ﬁnishing a race in the last 2 positions were 5.8 times more likely to be diagnosed with IAD. This ﬁnding was also conﬁrmed in Thoroughbreds, based on the signiﬁcant correlation of detection of moderate to severe grades of tracheal mucus with poor racing performance [137], and the negative correlation between BALF neutrophilia and successful racing [138]. In showjumpers and dressage horses, IAD does not seem to affect performance per se [14]; however, increased mucus scores have been associated with decreased willingness of these horses to perform [139]. Like its aetiology, the pathogenetic mechanisms of IAD leading to respiratory dysfunction at exercise still remain hypothetical. Respiratory functional studies have shown that IAD creates increased respiratory impedance and increased work of breathing at rest [140–143]. Use of the forced oscillation technique showed that there is reduced compliance and increased resistance in the lower frequency range (1–5 Hz) in horses with IAD compared with healthy horses, suggesting a heterogeneous lower airway ventilation, which may be caused by obstruction or thickening of the lung tissue [140,143]. These ﬁndings correlate with the histological evidence of bronchial epithelial hyperplasia found in the lower airways. Moreover, the severity score of lung biopsy samples was shown to correlate negatively with ventilatory parameters [133]. During submaximal exercise, racehorses with IAD have increased lactataemia in comparison with control horses [28,114,144]. Tidal volume and minute ventilation during intense exertion were lower [133] and respiratory effort increased in horses with IAD compared with healthy control animals [145]. A single study showed that horses with IAD displayed more severe hypoxaemia at submaximal levels of exercise than healthy control animals [144]. The arterial partial pressure of CO2 during exercise remained comparable between groups, thereby excluding hypoventilation as a cause of hypoxaemia. Ventilation–perfusion mismatching would thus be the most likely mechanism interfering with arterial oxygenation in horses with IAD. Airway hyperresponsiveness is another feature of IAD that may aggravate ventilation–perfusion mismatching and, in certain circumstances, contribute to poor performance [146]. Similar to RAO, signiﬁcantly higher PAP and systemic arterial mean pressure were measured during maximal exercise in horses with IAD in comparison with healthy animals [134]. In that study, an increase in red cell volume to body weight ratio was also found and interpreted as an adaptative response to exercise-induced hypoxaemia. Both hypoxaemic pulmonary vasoconstriction and increased haematocrit in horses with IAD may contribute to increased PAP. 380 E. Van Erck-Westergren et al. Exercise-induced pulmonary haemorrhage Exercise-induced pulmonary haemorrhage is a unique respiratory condition that results in the shedding of blood in the lungs and airways after strenuous exercise. In practice, the diagnosis is generally made by observation of post effort epistaxis or blood within the trachea and lower airways. The condition is ubiquitous in racehorse populations, where prevalence as high as 95% has been reported [147–149]. Horses performing in other disciplines, more generally those including intense or fast bouts of exercise, such as 3-day eventing or polo, have also been diagnosed with EIPH [150–152]. More recently, there have also been reports of EIPH in high-level showjumpers [153], in horses trotting at a submaximal pace up to fatigue [154]. There are only anecdotal cases reported in endurance horses [5] and almost none in leisure or dressage horses. The risk factors identiﬁed for EIPH are age and sex, the type and distance of race, the hardness of the ground and presence of jumps and the air temperature [147,155–159]. A major limitation to studying EIPH, and one that generates conﬂicting scientiﬁc results, is the absence of a reliable reference diagnostic method. A repeatable, quantitative technique to measure the severity of bleeding, map its anatomical distribution and determine its functional consequences in vivo is lacking. Such a technique would be an invaluable research tool [160,161]. The discrepancy between varying diagnostic methods may be illustrated by the comparison of similar studies undertaken to evaluate the prevalence of post race EIPH in Thoroughbreds; in one study, a single observation of epistaxis was used as a diagnostic method, and the condition was diagnosed in 0.15% of racehorses [156]; in other studies relying on endoscopic observation of tracheal blood, a positive diagnosis was made in 44–50% of horses [147,155,162]. To date, owing to the lack of a better alternative, post effort cytology of BALF is considered the best and most sensitive option for EIPH diagnosis [163]. It may include the counting of red blood cells (RBCs) and haemosiderophages, and also the measurement of the haemoglobin concentration of the sample [138,164,165]. However, although RBC counts in the BALF are alleged to be proportional to the severity of haemorrhage [164,166,167], the sampling is limited to a small portion of a single lung, and haemorrhage may be underestimated or even missed [168]. Given that unilateral lung bleeding has been observed from post mortem specimens, recommendations to sample both lungs have been made [169]. The negative impact of EIPH on performance has been demonstrated [170]. There are immediate and short-term factors that may impair lung function, such as the timing of the onset of bleeding in relation to beginning exercise and the effect of different volumes of haemorrhage within the alveoli, and longer term sequelae due to the repeated presence of blood in the airways and pulmonary interstitium. Decreased performance in horses diagnosed with EIPH has been shown in both Thoroughbred [157,166,170–173] and Standardbred racehorses [28,136]. As EIPH is frequently associated with other potential causes of poor performance, the relative role of each speciﬁc problem is difﬁcult to assess. Considering the structural and inﬂammatory consequences borne by EIPH-affected lungs, which are discussed hereafter, EIPH has a functional impact on the respiratory response to exercise. The pathophysiological mechanisms leading to EIPH are not fully elucidated. Multiple hypotheses have been proposed, but complex interactions are most likely to be responsible. Accumulated evidence indicates that EIPH results from the disruption of pulmonary alveolar capillary walls during exercise and only occasionally stems from bronchial capillaries [174–176]. Although the equine alveolocapillary wall is more resistant to shear forces than that of certain other species [177], its disruption is promoted during exertion by the occurrence of remarkable transmural pressures, beyond the rupture threshold of 75–100 mmHg [178,179]. High transmural pressures result from the summation of very negative alveolar pressures during inspiration and high positive capillary intravascular pressures. On the vascular side, pulmonary wedge pressures up to 80 mmHg have been measured during maximal exertion, which corresponds to an almost 3-fold increase in PAP compared with measurements made at rest [177,180–185]. A study measuring protein content in BALF of horses with EIPH also suggested that EIPH could in fact be a protein-rich ﬁltrate of blood rather than true haemorrhage [169]. The dramatic increase in haematocrit during exercise triggered by the release of splenic RBCs may substantially alter blood viscosity. This Equine Veterinary Journal 45 (2013) 376–387 © 2013 EVJ Ltd E. Van Erck-Westergren et al. phenomenon could contribute to pulmonary and systemic hypertension during exercise [186], although contradictory ﬁndings in vitro show that increases in pulmonary microvasculature pressure are unlikely to be related to changes in blood viscosity [187]. Mechanisms inﬂuencing pulmonary vascular pressures (PVP) play a fundamental role in the pathophysiology of EIPH. The severity of EIPH is positively correlated to high PAP [164,177,179]. Determinants of PVP may be haemorheological, cardiovascular or respiratory in origin. Several cardiovascular mechanisms also inﬂuence PAP during exercise. Cardiac output may reach extreme values at maximal exertion (>600 ml/kg/min in Thoroughbreds), producing physiologically high PAP [188]. High left-sided resistance also plays a role in increasing pulmonary hypertension. As a result of high heart rates, the relaxation time of the left ventricular myocardium is shortened, which leads to decreased compliance and pressure overload on pulmonary capillary walls [175]. The existence of cardiac disorders has the potential to disrupt haemodynamics further and may promote EIPH. Mitral and aortic valvular regurgitation and cardiac arrhythmias, such as atrial ﬁbrillation, have been shown to raise pulmonary wedge pressures above normal values at rest and during exercise [189–191]. Recently, other studies have demonstrated that downstream pulmonary veno-occlusive remodelling occurs in EIPH-positive horses [37,192]. This condition, attributable to chronic hypertensive episodes within the lung, as described above, would increase the chances of EIPH reoccurrence and explain the worsening of EIPH with age. Although hypoxic pulmonary vasoconstriction is a recognised cause of pulmonary hypertension and oedema in humans and cattle, it does not seem to be a contributory factor to pulmonary hypertension in horses [182,193]. Respiratory mechanics also appear to play a central role in the pathogenesis of EIPH. Intrathoracic pressures contribute substantially to modulating PAP in horses [194,195]. The observation of EIPH in horses exercising at submaximal levels supports the signiﬁcant contribution of extravascular factors [154,196]. Increased tidal volume observed in these horses would be associated with greater alveolar pressure swings, in a situation where PAP is lower than in maximally exerted horses [154,197]. Jones et al. [198] measured heterogeneous intrapleural pressure ﬂuctuations along the thorax in exercising and swimming horses. They showed that the caudodorsal region of the thorax experienced larger pressure oscillations than other regions, and post mortem and histopathological studies have demonstrated that EIPH occurs precisely in that region [199,200]. Ventilation heterogeneity is also accompanied by regional variations in perfusion [201,202]. During exercise, blood ﬂow increases primarily in the dorsal-caudal region of the lung [188]. These ﬁndings are associated with the observation of a greater ventilation–perfusion mismatch in the caudodorsal pulmonary region during exercise [200]. Physiologically, upper airway resistance represents over 90% of total respiratory resistance during exercise [203]. Further increases in inspiratory airway resistance, for instance by induction of laryngeal hemiplegia [193] or nasal obstruction [195], lead to more negative oesophageal (or transpulmonary) pressure and a subsequent increase in transmural capillary pressures that might further promote EIPH. Detection and resolution of dynamic upper airway obstruction is essential in managing horses suffering from EIPH. Other possible causative or aggravating factors leading to EIPH have been suggested. The theory of the impact of locomotion-induced shock waves on the caudodorsal area of the thorax has been proposed by Schroter et al. [204]. This theory is based on the traumatic effect of successive shock waves generated by foot impact and travelling across the thorax to concentrate in the peripheral caudodorsal area of the lung. It is supported by the high incidence of EIPH in horses racing over obstacles or on hard ground, but cannot alone account for the pathogenesis of EIPH [156]. Exercise-induced pulmonary haemorrhage (epistaxis) occurs in swimming horses [205]. However, Watkins et al. [206] reported that there were no records of epistaxis post swimming in over 150,000 swimming events during the 2004–2005 race season in Hong Kong. Mean pulmonary arterial and right atrial pressures during swimming are similar to those of horses that experience EIPH when running near maximal oxygen uptake on a treadmill; hence, it was suggested that the smaller subatmospheric intrapleural pressure excursions during swimming result in smaller Equine Veterinary Journal 45 (2013) 376–387 © 2013 EVJ Ltd Responses of horses with respiratory disease to exercise transmural pressures associated with capillary stress failure in the lungs [207]. Changes in thoracic morphology and the application of excessive asymmetrical compressive forces over the lungs have been suggested as cofactors for the development of EIPH [208]. Haemostatic and morphological erythrocyte abnormalities have not been identiﬁed consistently in horses with EIPH, although some degree of inhibition in platelet function has been detected [209]; however, these ﬁndings have not been substantiated [210], and the signiﬁcance of platelet dysfunction, if any, is unknown. Although it is improbable that it is a primary cause of EIPH, it may lengthen bleeding time within the lungs. The association between EIPH and IAD has been considered periodically, with varying theories concerning which problem might be the primum movens [136,171,211]. Correlation has been found between inﬂammatory BALF cytology and pulmonary histopathology proﬁles [212]. On the basis of BALF evaluation, several investigators have concluded that naturally occurring EIPH or simulated EIPH induced by autologous blood instillation elicited mild but prolonged inﬂammation [168,213–216]. Pre-existent lower airway inﬂammation also promotes the occurrence of EIPH [217]. In the longer term, the presence of blood in the airways stimulates an inﬂammatory response that may lead to permanent ultrastructural sequelae in the lung [199,200,218,219]; these include bronchiolitis, connective tissue ﬁbrosis, neovascularisation and other vascular lesions consistent with chronic hypertension [37,192,196,200]. These lesions of the small airways alter pulmonary mechanical properties and cause an increase in respiratory resistance as well as a decrease in compliance [4,213,216]. They also increase the risks of recurrence of EIPH [37]. During exercise, the functional consequences of EIPH include a worsening of arterial hypoxaemia and hypercapnia [114,144] and a decrease in maximal oxygen uptake at supramaximal exertion [220,221]. Pre-existent lung disease caused by infectious or environmental stress is potentially also deleterious to EIPH-affected horses [211]. Anti-inﬂammatory treatment has been advocated to limit EIPH-induced inﬂammation [217,222]. Furosemide is one of the few drugs that have proven effects in reducing EIPH [223]. In several countries, furosemide is used extensively in horses with EIPH, and its use is authorised during competitions, although such use is controversial because of its perceived performance-enhancing properties. Administration of furosemide 4 h prior to exercise reduces EIPH by up to 90% in Thoroughbred racehorses running at 95% of maximal oxygen uptake [163]. Right atrial, pulmonary arterial, pulmonary wedge and pulmonary capillary pressures are signiﬁcantly reduced, as are the post effort RBC concentrations in the BALF [184]. The demonstrated haemodynamic effects of furosemide include a redistribution of pulmonary blood during exercise from the dorsal portion of the lung to the ventral parts, as well as vasodilatory activities that promote an increase in venous capacitance [224]. These effects reduce venous return to the atria and cardiac ﬁlling, hence they reduce pulmonary venous pressure. However, it has been suggested that most of the ergogenic properties of furosemide in racehorses may be due simply to diuretic weight loss [225,226]. The use of equine nasal strips has been shown to alleviate inspiratory resistance and decrease the severity of EIPH [163,227]. Conclusions The metabolic adaptations of skeletal muscle and the cardiovascular system have resulted in a physiological situation in athletic horses of various types in which performance is limited by the capacity of the respiratory system [1], especially in the presence of even mild or subclinical disease. Respiratory or ventilatory capacity is determined by the ability to facilitate high-frequency ventilation of the lungs with large volumes of air and the exchange of oxygen and carbon dioxide at the bronchoalveolar–pulmonary capillary interface. In even the healthiest and best performing of these horses, ventilation is relatively inadequate when considered in terms of the oxygen consumed and the carbon dioxide produced at these performance levels. For these reasons, hypercapnia and hypoxaemia, and the associated desaturation of haemoglobin with oxygen, are the norm in ﬁt, healthy racehorses performing at moderate to high intensities. Hypoxaemia begins to develop at about 60% of maximal oxygen uptake, while hypercapnia is ﬁrst detected at 85–90% of maximal oxygen uptake [1]. 381 Responses of horses with respiratory disease to exercise In some cases, even mild perturbations in any part of the airway and/or gas exchange segments of the lungs can have major effects on airﬂow, ventilation, gas exchange and performance, especially when considering horses competing at levels that require maximal aerobic capacity. These abnormalities have been linked to a wide variety of anatomical and/or inﬂammatory conditions. Some are only detectable or clinically relevant during strenuous exercise, which makes the task of detecting and managing them a challenge. In many cases, a diagnosis cannot be made conﬁdently without involving an exercise test in the diagnostic evaluation of the patient. The last 2 decades have witnessed major improvements in the understanding of the ventilatory responses of horses to exercise and the diagnosis and treatment of the many maladies of the respiratory tract that interfere with optimal performance. Equine veterinary practice is now poised to transpose this knowledge from controlled laboratory situations to the ﬁeld via the application of the newest diagnostic technologies. This advent should facilitate further improvement in diagnostic capabilities and treatments of upper airway conditions in particular, and should be welcomed by equine exercise scientists, horsemen and veterinarians alike. Authors’ declaration of interests No conﬂicts of interest to declare. 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J. 43, 179-182. 221. McKane, S.A., Bayly, W.M., Sides, R.H., Kingston, J.K. and Slocombe, R.F. (2008) Effects of pre-exercise intrapulmonary blood inoculation on equine pulmonary function during supramaximal exercise. Comp. Exerc. Physiol. 5, 7-13. 222. Walker, H.J., Evans, D.L., Slocombe, R.F., Hodgson, J.L. and Hodgson, D.R. (2006) Effect of corticosteroid and bronchodilator therapy on bronchoalveolar lavage cytology following intrapulmonary blood inoculation. Equine Vet. J. Suppl. 36, 516-522. 223. Hinchcliff, K.W., Morley, P.S. and Guthrie, A.J. (2009) Efﬁcacy of furosemide for prevention of exercise-induced pulmonary hemorrhage in Thoroughbred racehorses. J. Am. Vet. Med. Assoc. 235, 76-82. 224. Olsen, S.C., Coyne, C.P., Lowe, B.S., Pelletier, N., Raub, E.M. and Erickson, H.H. (1992) Inﬂuence of furosemide on hemodynamic responses during exercise in horses. Am. J. Vet. Res. 53, 742-747. 225. Bayly, W.M., Slocombe, R.F., Schott, H.C. and Hodgson, D.R. (1999) Effect of intravenous administration of furosemide on mass-speciﬁc maximal oxygen consumption and breathing mechanics in exercising horses. Am. J. Vet. Res. 60, 1415-1422. 226. Zawadzkas, X.A., Sides, R.H. and Bayly, W.M. (2006) Is improved high speed performance following frusemide administration due to diuresis-induced weight loss or reduced severity of exercise-induced pulmonary haemorrhage? Equine Vet. J. Suppl. 36, 291-293. 227. Geor, R.J., Ommundson, L., Fenton, G. and Pagan, J.D. (2001) Effects of an external nasal strip and frusemide on pulmonary haemorrhage in Thoroughbreds following high-intensity exercise. Equine Vet. J. 33, 577584. NEW TITLE ! EVJ BOOKSHOP Respiratory Diseases of the Horse L.L. Couetil & J.F. Hawkins Publisher: Manson, March 2013 • Hardback 256 pages The authors provide a problem-oriented approach to the assessment and management of respiratory illness in horses. The book deals first with the anatomy, function and clinical examination of the respiratory system, followed by discussion of diagnostic tests and procedures. The clinical section is focused around the cardinal presenting manifestations of equine respiratory disease: coughing, nasal discharge, increased breathing efforts, respiratory noise, plus a chapter on congenital abnormalities. The text is presented systematically covering definition, aetiology, pathophysiology, clinical presentation, differential diagnoses, diagnosis, management and treatment. EVJ price: £80 plus p&p BEVA member price: £72 plus p&p The book is illustrated throughout with excellent quality colour photos, diagrams and algorithms. It is of lasting value to equine specialists in practice and in training, and will be a useful reference for non-specialist practitioners. EVJ Bookshop, Mulberry House, 31 Market Street, Fordham, Ely, Cambs. CB7 5LQ, UK Tel: 01638 723555 ! Fax: 01638 724043 ! Email: bookshop@evj.co.uk ! www.beva.org.uk Equine Veterinary Journal 45 (2013) 376–387 © 2013 EVJ Ltd 387

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