Chapter 9 Cor Pulmonale and Pulmonary Thromboembolism
INTRODUCTION
Cor pulmonale is defined as right-heart failure caused by pulmonary or thoracic disease. It may be characterized by clinical signs of fluid accumulation or by radiographic or echocardiographic evidence of right ventricular overload. By definition, pulmonary hypertension (PH) must be present in cor pulmonale in order for the right heart to fail. Heartworm disease with pulmonary vascular obstruction is the most common cause of cor pulmonale in the canine population, although any pulmonary vascular obstruction has the potential to result in PH and cor pulmonale. Pulmonary arterial obstruction can result from lodging of clot material (pulmonary thromboembolism [PTE]) or from embolization of fat, septic material, neoplastic cells, or heartworms in the pulmonary arteries or capillary bed.
COR PULMONALE AND PULMONARY THROMBOEMBOLISM
Physiology
• Pulmonary circulatory pressures are maintained at a level much lower than systemic pressures in order to reduce the workload on the thin-walled right ventricle. Normal pressures in the dog and cat are reported as a systolic pulmonary artery pressure of 15 to 25 mm Hg, end-diastolic pulmonary artery pressure of 5 to 10 mm Hg, and a mean pulmonary artery pressure of 10 to 15 mm Hg. The pulmonary circulation maintains low right ventricular pressure in the face of increases in cardiac output through recruitment of closed capillaries and distension of existing capillaries.
• Distribution of pulmonary blood flow is altered by hypoxic pulmonary vasoconstriction and is also modulated by endothelial release of vasoconstrictors and vasodilators. Hypoxic pulmonary vasoconstriction is a protective mechanism that prevents de-oxygenated blood from entering the circulation by preferentially constricting vascular supply to poorly ventilated lung regions. Thus, local alveolar hypoxia results in local vascular constriction that preserves gas exchange. However, global hypoxia or diseases that disrupt the normal response to hypoxia can result in a deleterious rise in pulmonary artery pressure. Alterations in endothelium-derived mediators can also impact pulmonary artery pressures. The most potent vasoconstrictor is endothelin-1; thromboxane A2 and superoxide also mediate vasoconstriction. Vasodilators produced by the endothelium include nitric oxide and prostacyclin. Release and activity of these vasoreactive mediators can be altered in disease states, and imbalance among the various mediators can result in a rise in pulmonary artery pressure.
• 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.
Clinical Presentation
History and Clinical Signs
• Dogs or cats with PH and cor pulmonale can be of any age, depending on the underlying etiology of elevated pulmonary artery pressures. Generally there is a history of signs referable to the pulmonary system or to congestive failure. Animals can display any combination of signs including lethargy, weakness, cough, respiratory distress, tachypnea, abdominal distention, and syncope. Historical features and clinical signs are not specific for PH or cor pulmonale but instead reflect the underlying cardiopulmonary disease.
• PTE is generally a disorder of older animals, and history and clinical signs reflect the underlying disease process. Difficulty in clinical recognition of this disorder is high, and animals with PTE are often presented for signs of weight loss, lethargy, and anorexia rather than for respiratory signs, although tachypnea is often present on admission. Secondary PTE should be suspected in an animal with a predisposing condition that develops an acute onset of tachypnea, cyanosis, and/or hypoxemia that is refractory to oxygen therapy.
Physical Examination
• Animals with cor pulmonale will generally display tachypnea or respiratory distress due to fluid accumulation (ascites or pleural effusion) or because of underlying pulmonary disease. A systolic heart murmur due to mitral or tricuspid regurgitation is found in the majority of dogs with PH. Animals that develop clinical signs of overt right-heart failure will display jugular venous distention, ascites, or subcutaneous edema.
• Dogs and cats with PTE have tachypnea and hyperpnea that is not alleviated by oxygen administration. Cough is relatively uncommon. Harsh lung sounds or loud bronchovesicular sounds can be detected; however, crackles or wheezes are less common. Physical examination abnormalities will reflect the underlying disease, such as pale mucous membranes in the case of immune mediated hemolytic anemia or a pot-bellied appearance due to Cushing’s disease.
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