PULMONARY HYPERTENSION is increased blood pressure in the pulmonary vascular system. In the past, the most common cause of pulmonary hypertension in dogs was heartworm infestation. The mechanical and immunologic effects of the worms can lead to various degrees of increased pulmonary vascular resistance and pressure. The widespread use of heartworm preventives has presumably reduced the frequency of pulmonary hypertension. However, nonheartworm-related pulmonary hypertension is also a clinical problem. Practitioners can now more easily distinguish between heartworm-related and nonheartworm-related cases by knowing a patient's heartworm prevention history and the results of heartworm antigen testing and echocardiographic examination.
Regardless of the cause, echocardiography can often noninvasively estimate intravascular and intracavitary pressures as well as identify morphologic cardiac changes in dogs with various degrees of pulmonary hypertension.1 This ability to quickly and easily identify cases of pulmonary hypertension has been an important diagnostic advance and has greatly reduced the need for cardiac catheterization.
Canine pulmonary hypertension ranges widely in severity. Pulmonary hypertension associated with left heart failure is usually mild, whereas dogs with advanced pulmonary disease can have peak systolic pressures in the right ventricle and pulmonary artery that are four to five times normal (normal = 20 to 25 mm Hg). In our laboratory, the estimated pressures are categorized as mild (30 to 55 mm Hg), moderate (56 to 79 mm Hg), and severe (> 79 mm Hg).
This article presents two cases of older dogs with severe pulmonary hypertension. These dogs had peak right ventricular systolic pressures in excess of 79 mm Hg, and their cases highlight three important aspects of pulmonary hypertension:
1. The difficulty in understanding the primary cause and pathophysiology of this life-threatening condition.
2. The cardiac manifestations of severely elevated pulmonary vascular pressure (cor pulmonale).
3. The challenge of planning and implementing a therapeutic protocol.
A 14-year-old, 36.4-lb (16.5-kg), mixed-breed, spayed female dog was presented to the referring veterinarian with a history of acute dyspnea, coughing, and anorexia. Auscultation of the lung fields had revealed diffuse crackles. The results of a heartworm antigen test done eight months earlier were negative, and the dog had been receiving a monthly heartworm preventive. The veterinarian had suspected that the dog had congestive heart failure and had instituted treatment with furosemide, enalapril, and oxygen before referral to the Veterinary Teaching Hospital at Virginia Tech.
1. This right short-axis echocardiogram demonstrates the thickened right ventricular free wall (arrows), the large right ventricle (RV), and the flattened interventricular septum (arrowheads) of the dog in Case 1. The displacement of the septum to the left and the diminished blood flow through the pulmonary vascular system can combine to cause the left ventricle (LV) to be smaller than normal.