Case Studies In Small Animal
Text from "Small Animal Cardiovascular Medicine"
CONSTRICTIVE AND CONSTRICTIVE-EFFUSIVE PERICARDITIS
Restriction of cardiac filling may occur as a result of reduced pericardial compliance involving the parietal pericardium, the visceral pericardium (epicardium), or both. In some cases, a small amount of pericardial fluid, although not enough to cause signs of tamponade if the pericardium were normal, may accompany constrictive pericarditis (constrictive-effusive pericarditis). In the authors experience the latter form is more frequently recognized in dogs. Constrictive pericarditis usually occurs as a result of thickening and fibrosis of the parietal pericardium secondary to an inflammatory process. With time the epicardium also becomes thickened and fibrotic and may fuse with the parietal pericardium causing obliteration of the pericardial space. Reported causes in dogs include recurrent IHPE, intrapericardial foreign bodies, chronic septic pericarditis, intrapericardial neoplasia, and traumatic pericardial hemorrhage. Constrictive pericarditis has been reported in a cat with dilated cardiomyopathy. The cause of constrictive pericarditis cannot be determined in most cases at the time of diagnosis. In humans, most constrictive pericardial disease is the result of an infectious process or neoplasia.
History and Physical Exam
Presenting complaints and physical findings are quite similar to pericardial effusion. Ascites is the most common. Less common clinical signs include dyspnea, tachypnea, fatigue, weakness, syncope, and weight loss. Most reported cases have involved middle-aged, large breed dogs. The clinical signs have often been present for weeks to months. Occasionally there is a history of previous IHPE. The most consistent clinical findings are ascites and jugular venous distension, although jugular distension is not a consistent feature. The femoral pulse is often weak, but pulsus paradoxus is rarely observed. Diminished heart sounds may be identified but less commonly than with PE. Other auscultatory findings may include a gallop sound, a systolic murmur, or a systolic click. These are usually not due to the constrictive pericarditis but are related to concurrent disease. The prominent pericardial knock commonly heard in people is uncommonly detected in dogs.
Electrocardiography, Radiography, and Echocardiography
The electrocardiographic findings in constrictive pericarditis are nonspecific, yet may aid in the diagnosis. Pericardial fibrosis tends to diminish QRS voltage similar to PE, however, to a lesser degree and with less consistency. Electrical alternans has not been reported in dogs with constrictive pericarditis. A right ventricular hypertrophy pattern has been reported in one dog with coccidioidomycosis and is a common electrocardiographic feature in human patients. Sinus tachycardia is the most commonly reported arrhythmia in dogs although other supraventricular arrhythmias are common in people.
Thoracic radiographs may or may not aid the diagnosis of constrictive pericarditis. Mild cardiomegaly may be identified with or without rounding of the cardiac silhouette. However, these findings are neither as dramatic nor as frequently identified as with PE. The caudal vena cava is commonly dilated, especially in dogs with moderate to severe ascites. Pleural effusion may be present. As with PE, fluoroscopic evaluation may demonstrate diminished or absent motion of the cardiac borders.
The echocardiographic diagnosis of constrictive pericarditis without an effusion is very difficult, and cardiac catheterization is usually required for an accurate diagnosis. In most cases, the diagnosis is based on the presence of clinical signs of cardiac tamponade with only a very small amount of pericardial effusion identified echocardiographically. If pleural effusion is present and the pericardium is outlined, it may appear thickened. Subtle abnormalities on the M-mode tracing have been reported in humans with constrictive pericarditis including flattened diastolic left ventricular posterior wall motion and abnormal systolic septal motion, but these findings have not been evaluated in dogs or cats. Doppler echocardiography may be helpful for identifying constrictive physiology and may be able to distinguish pericardial and myocardial disease. Pulsed-wave Doppler evaluation of systemic venous, hepatic, or pulmonary venous flow often shows characteristic changes in blood flow velocity in humans.
Although noninvasive studies may be supportive, the definitive diagnosis of constrictive pericarditis often requires cardiac catheterization. Central venous pressure is invariably elevated and mean atrial and diastolic ventricular pressures are usually high. Simultaneous recordings of atrial and ventricular pressures often show equilibration and superimposition of diastolic pressures. In some dogs, a prominent early diastolic dip and mid diastolic plateau ("square root sign) may infrequently be identified on ventricular pressure tracings. The lack of consistency of this finding compared to humans may reflect the fact that many dogs with constrictive pericarditis have a small amount of pericardial fluid (constrictive-effusive pericarditis). Some dogs show surprisingly normal catheterization studies and the above findings are only evident after rapid fluid loading with a crystalloid solution.
Therapy and Prognosis
The temporary benefits and potential adverse effects of medical therapy (diuretics and venodilators) provide little value for the treatment of constrictive pericarditis. Successful treatment invariably requires surgical removal of the fibrotic pericardium. When the epicardium is minimally involved, subtotal pericardiectomy is relatively easy and highly successful for controlling the clinical signs of congestive right heart failure. However, when the epicardium is also fibrotic and thickened, epicardial stripping, a more difficult procedure, is required. There is a high degree of morbidity and mortality associated with epicardial stripping and the results are generally less favorable than those controlled by pericardiectomy alone.
©Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.