Severe pulmonary hypertension and cardiovascular sequelae in dogs - Veterinary Medicine
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Severe pulmonary hypertension and cardiovascular sequelae in dogs
Once thought to be caused mostly by dirofilariasis, pulmonary hypertension is still being seen despite heartworm preventive measures, signifying additional important causes. Technologic advances may help us recognize the signs in time.


Further diagnostic tests and treatment

The dog continued to cough, had limited exercise tolerance, and was weak in the first few days after surgery. Continuous nasal oxygen insufflation was provided. Other therapies included carprofen (2.4 mg/kg b.i.d.), levothyroxine (0.016 mg/kg b.i.d.), theophylline (9.7 mg/kg t.i.d.), amoxicillin (23 mg/kg t.i.d.), and intravenous fluids. Several cardiovascular evaluations were done during the postoperative period.

4A. This lateral thoracic radiograph of the dog in Case 2 shows moderate cardiomegaly. The trachea is elevated. There are multiple small radiopaque lesions most visible over the heart shadow. These small opacities were considered to be age-related and not necessarily linked to pulmonary hypertension.
Five days after the surgery, physical examination revealed increased frequency of coughing; loud, bilateral pulmonary crackles; and one episode of collapse. Three blood gas analyses were done during this period, and the partial pressure of oxygen (PO2) in arterial blood averaged 58 mm Hg (normal = 84.7 to 116.1 mm Hg). An electrocardiographic examination revealed frequent ventricular premature beats with an occasional three-consecutive-beat pattern (intermittent ventricular tachycardia). Thoracic radiographs showed right ventricular enlargement and an enlarged pulmonary artery (Figures 4A & 4B).

4B. This dorsoventral thoracic radiograph presents a classic reversed D sign due to right ventricular hypertrophy. At the 2-o'clock location, there is an enlarged pulmonary artery segment.
Echocardiographic findings were dramatically changed from the original examination five days earlier. The right ventricle was enlarged, and the interventricular septum was flattened. The left ventricular diameter from the right short-axis view was markedly diminished. The right short-axis M-mode diastolic diameter was 2.58 cm (normal = 4.3 cm), and the systolic diameter was 0.7 cm (normal = 2.8 cm). There was substantial tricuspid and pulmonary valve regurgitation. The right ventricular free wall was thicker (1.48 cm) than the left ventricular free wall (1.41 cm).

5. A photomicrograph of a specimen from the lung of the dog in Case 2. There is marked tunica adventitia thickening and mild tunica media thickening in the pulmonary artery. In addition, there is marked inflammatory reaction compatible with infectious or inflammatory pulmonary disease (hematoxylin-eosin).
Using the tricuspid jet peak velocity measurement, spectral Doppler echocardiography, and the modified Bernoulli equation, we determined that the peak systolic right ventricular and pulmonary artery pressures were about 100 mm Hg. Using the end-diastolic velocity, spectral Doppler echocardiography, and the modified Bernoulli equation, we determined the end-diastolic pulmonary artery pressure was at least 20 mm Hg (normal = 10 mm Hg). In an effort to reduce pulmonary vascular resistance and pressure, treatment with an α-adrenergic blocking agent (2 mg prazosin hydrochloride orally t.i.d.) was begun.2 In two subsequent echocardiographic examinations done six and eight days postoperatively, the right ventricular and pulmonary artery pressures remained severely increased. Additional therapy included prednisone (0.5 mg/kg orally once a day) and enrofloxacin (5 mg/kg orally b.i.d.). The prednisone was given to reduce inflammatory changes and swelling in the upper and lower respiratory tract in an effort to improve gas exchange. The enrofloxacin was used because of a concern that the dog might aspirate gastric contents. Blood gas analysis continued to reveal low PO2 levels.

Nine days after surgery, the dog was discharged from the hospital. The owner was told that the prognosis was poor because of severe pulmonary hypertension and general unresponsiveness to therapy. The therapeutic plan at discharge included enrofloxacin (5 mg/kg orally b.i.d.), amoxicillin (23 mg/kg orally t.i.d.), prazosin (2 mg orally t.i.d.), and prednisone (0.25 mg/kg orally b.i.d.). The carprofen and levothyroxine were discontinued.


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