Clinical Exposures: Pulmonary thrombosis due to idiopathic main pulmonary artery disease - Veterinary Medicine
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Clinical Exposures: Pulmonary thrombosis due to idiopathic main pulmonary artery disease

Figure 1A. The referring veterinarian obtained these thoracic radiographs when the dog was experiencing severe respiratory distress. In the lateral view (1A), the cardiac silhouette is enlarged, particularly in the cranial-caudal dimension (four intercostal spaces), and sternal contact is increased because of right ventricular enlargement. A mixed interstitial and alveolar pattern is present in the lung fields and tends to have a central distribution. The bronchi appear enlarged, and the accompanying vessels appear small.
A 10-year-old 35.9-lb (16.3-kg) intact female Wheaton terrier was referred to the teaching hospital at Virginia Tech for evaluation of dyspnea. The dog was accustomed to running long distances with its owner, and four days earlier the dog had run three miles. Two days after the run, the dog had collapsed after mild exercise and may have experienced a seizure. The dog had recovered from this episode within minutes, and its appetite had been normal later that day.

Within the next 24 hours, the owner had noticed that the dog was having breathing difficulties and occasional coughing episodes. He took the dog to his veterinarian. The dog's vaccinations were current, and it was receiving a monthly heartworm preventive. The veterinarian's physical examination had revealed increased respiratory effort. A complete blood count had revealed a lymphopenia and a mature neutrophilia consistent with a stress response. A serum chemistry profile had revealed mildly elevated alkaline phosphatase activity (263 IU/L; normal = 0 to 140 IU/L).

The dog had been discharged from the clinic, but during the next 24 hours its respiratory signs had worsened, so the owner had returned the dog to the veterinarian. The second physical examination had revealed severe respiratory stridor with weakness and listlessness. Substantial pulmonary and cardiac abnormalities were identified on thoracic radiographs (Figures 1A & 1B). That same day, the veterinarian referred the dog to the Virginia Tech teaching hospital.

Evaluation and treatment

Figure 1B. In the dorsoventral view (1B), the right ventricular silhouette is prominent (reversed D), as is the pulmonary artery segment (1- to 2-o’clock position). The middle right lung lobe and caudal part of the cranial left lung lobe have increased opacity, possibly due to pulmonary edema.
At Virginia Tech, physical examination revealed severe respiratory distress including dyspnea and tachypnea (60 breaths/min). The dog held its neck in extension, and the elbows were abducted. The dog's heart rate was 140 beats/min, and its rectal temperature was 98.1 F (36.7 C). On thoracic auscultation, bilateral wheezes and crackles were heard throughout the lung fields. The dog was in critical condition, so the physical examination was abbreviated, and the dog was transported to the intensive care unit (ICU).

Figure 2. This echocardiogram was obtained with the dog positioned right side down and shows the heart in a right, short-axis presentation. The right ventricle (RV) is greatly enlarged by pressure and volume overload. The interventricular septum is displaced to the left, giving it a flattened appearance and causing the left ventricle (LV) to have a triangular shape. The left ventricle is smaller than normal because of the reduced pulmonary venous return to the left heart (RVW = right ventricular wall [between arrows]; RVOT = right ventricular outflow tract).
The dog was placed in an oxygen cage. Within minutes, cardiac arrest occurred, and the dog was resuscitated by administering 3.3 ml 1:1000 epinephrine intravenously and providing standard cardiopulmonary support. In addition, furosemide (1.2 mg/kg) was given intravenously for suspected pulmonary edema, and atropine (0.033 mg/kg) was given intravenously. While the dog was being prepared for echocardiography, there was a second cardiac arrest and successful resuscitation. An abbreviated echocardiographic examination, including spectral Doppler imaging, was performed in the ICU, and features compatible with pulmonary hypertension were apparent (Figure 2). Peak right ventricular systolic pressure was derived by converting the peak tricuspid regurgitant jet velocity (m/sec) to pressure by using the Bernoulli equation1 and was at least 97 mm Hg (normal = 20 to 30 mm Hg). There was no evidence of primary cardiac disease, including pulmonic stenosis. As the echocardiographic examination was being completed, cardiac arrest occurred for the third time, but efforts to resuscitate the dog were unsuccessful.


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