A number of different theories have been proposed to explain the occurrence of exercise-induced pulmonary hemorrhage, however few, if any, have been able to explain the initial site of occurrence and pattern of progression of hemorrhage through the lung. The most widely accepted theory at present is that of pulmonary capillary stress failure resulting from high transmural pressures (i.e., pressures or stresses acting on the pulmonary capillaries). Pulmonary capillary transmural pressure is determined by pulmonary capillary pressure and airway pressure. The horse has high pulmonary vascular pressures during intense exercise. When the high pulmonary vascular pressures (exceeding 100 mm Hg) distending the blood vessels are opposed by high positive airway pressures, such as occur during expiration, the transmural pressure and, by implication, wall stress is low. However, when the distending internal vascular pressure coincides with a large negative airway pressure, as occurs during inspiration, the transmural pressure and therefore wall stress is high.
Studies in vitro have demonstrated that significant disruption of the pulmonary capillaries occurs at pressures of at least 80 mm Hg. One study demonstrates an in vivo threshold mean pulmonary artery pressure of around 80 to 95 mm Hg, above which significant hemorrhage is more likely to occur. On the basis of this theory, any factor or disease that increases pulmonary vascular pressures, such as hypervolemia, or increases the magnitude of the negative pressures in the lung during inspiration, such as dynamic upper airway obstruction, would be expected to increase the severity of exercise-induced pulmonary hemorrhage. Neither experimentally induced laryngeal hemiplegia nor dorsal displacement of the soft palate increases pulmonary capillary transmural pressure. The limitation of the pulmonary capillary stress failure theory is that it does not in itself explain the site or pattern of progression of exercise-induced pulmonary hemorrhage.
More recently a new theory for exercise-induced pulmonary hemorrhage has been proposed based on locomotory forces. This theory claims to explain the site of initiation in the tips of the dorsocaudal lung, the nature of the damage, and the pattern of progression. The theory is based on the fact that during galloping, the absence of any bone attachment of the forelegs to the spine causes the shoulder to compress the cranial rib cage. The compression occurs largely during the stance phase when the limb is planted on the ground and the body swings over the limb. The shoulder is moved in a dorsal and cranial direction into the chest. The compression of the chest initiates a pressure wave of compression and expansion that spreads outward. However, because of the shape of the lung and reflections off the chest wall, the wave of expansion and compression becomes focused and amplified in the dorsocaudal lung. The alternate expansion and compression at the microscopic level in adjacent areas of lung tissue creates shear stress and capillary disruption. The notion that hemorrhage could occur in the lung in this way is consistent with the type of hemorrhage resulting from blunt trauma to the front of the chest or head, which commonly results in lung or brain damage; hemorrhage in car accident victims; and hemorrhage in boxers. In both accident victims and boxers the hemorrhage occurs at the opposite side of the body to that which is initially struck. The theory predicts that hemorrhage would be more severe on hard track surfaces. At present this theory has not been investigated.
The relationship between exercise-induced pulmonary hemorrhage and airway inflammation is controversial. Two studies have shown that exercise-induced pulmonary hemorrhage severity does not correlate with airway inflammation as judged by bronchoalveolar lavage cytology, airway obstruction, or airway reactivity. Furthermore, airway inflammation, not exercise-induced pulmonary hemorrhage, is associated with reduced performance, leading to the notion that exercise-induced pulmonary hemorrhage and lower airway inflammation are distinct entities. In contrast, recent surveys in Thoroughbred racehorses, using tracheal wash cytology as a measure of inflammation, showed an increased risk for exercise-induced pulmonary hemorrhage with greater inflammation (unpublished data). The link between exercise-induced pulmonary hemorrhage and inflammatory airway disease requires further study. In summary, a pragmatic view of exercise-induced pulmonary hemorrhage may be that it is a multifactorial condition that involves airway, vascular, and locomotory components.