Chapter 9 Cor Pulmonale and Pulmonary Thromboembolism
COR PULMONALE AND PULMONARY THROMBOEMBOLISM
Physiology
• PTE results in abnormal gas exchange, altered vascular control, changes in pulmonary mechanics, and loss of ventilatory control. Physical obstruction of large pulmonary arteries leads to increased vascular pressure and reactive pulmonary vasoconstriction from release of clot associated factors such as thromboxane that increase vascular resistance. Secondary alterations in pulmonary physiology worsen and perpetuate derangements in gas exchange. Release of humoral mediators such as serotonin from platelets results in bronchoconstriction and increased airway resistance. Surfactant function is altered leading to loss of elastic recoil and atelectasis, decreased pulmonary compliance, and increased right-to-left shunting. Work of breathing increases because of augmented alveolar dead space from nonperfused lung regions.
Etiology
• Cor pulmonale can result from disorders that impact the pulmonary vasculature, such as obstructive or obliterative diseases of the pulmonary circulation, or sustained hypoxic vasoconstriction associated with chronic parenchymal or tracheobronchial disease. Rarely, an increase in pulmonary blood flow will result in PH. Not all animals with associated disorders will develop PH and cor pulmonale, and it is likely that genetic or other influences will determine the vascular response. PH and cor pulmonale appear to be encountered more commonly in dogs than in cats. Primary PH is relatively uncommon; however, various pulmonary conditions can lead to secondary PH in the dog or cat, including chronic tracheobronchial disorders, pneumonia, or interstitial lung disease (Box 9-1). A minority of these animals will develop overt clinical signs of right-heart failure.
• PTE is a secondary condition that occurs in association with diseases that cause blood stasis, alter endothelial integrity, or increase coagulability. PTE has been linked most commonly with immune-mediated hemolytic anemia, neoplasia, sepsis, protein losing nephropathy, cardiac disease, and hyperadrenocorticism (Box 9-2). Clinically silent pulmonary embolism occurs in a majority of dogs (82%) undergoing total hip replacement surgery. Small pulmonary thromboemboli are rapidly lysed and removed by the local fibrinolytic system; however, occlusion of larger pulmonary arteries or massive showering of emboli to a large circulatory volume can lead to acute right ventricular overload.