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.


Treatment and outcome

While it was appreciated that pulmonary parenchymal disease could be the underlying problem in this dog, the immediate threat was the severe pulmonary hypertension. Thus, the therapeutic plan included steps to reduce pulmonary vascular resistance and pressure. Therapy included 40% cage oxygen, sildenafil citrate (we decided to administer a dosage of 1.5 mg/kg orally b.i.d. and gradually increased it over five days to 6 mg/kg every four to six hours), and heparin (100 U/kg subcutaneously q.i.d.).

Repeated echocardiographic studies were done to assess the effectiveness of the therapy. While some peak right ventricular systolic pressure measurements were as low as 50 mm Hg, the pressure never consistently remained reduced, and the dog did not improve clinically. After five days of continuous oxygen therapy, increasing doses of sildenafil (maximum dose of 6 mg/kg orally four to six times a day), heparin, amoxicillin (24 mg/kg b.i.d., added on Day 3), and furosemide (3 mg/kg t.i.d., added on Day 4), the dog was euthanized.

3. A photomicrograph of a specimen from the lung of the dog in Case 1. The two pulmonary arteries in this section demonstrate advanced arteriosclerosis. There is marked thickening of the tunica media and tunica adventitia. The thickening of the tunica media is due to proliferation of muscle fibers, and there is increased fibrous tissue in the tunica adventitia. The vascular thickening is presumably an important factor in the development of pulmonary hypertension (hematoxylin-eosin).
A complete necropsy was performed. The lungs were mottled and rubbery, and the lung peripheries were firmer than the hilar portions. No thrombi were present in the pulmonary arteries. The heart was dilated with a hemorrhagic right auricle. The kidneys were grossly normal. Histologically, the kidneys showed scattered interstitial areas that were infiltrated with lymphoid cells. Pulmonary alveoli were filled with neutrophils and macrophages, and some contained fibrin. Many of the smaller pulmonary arteries were thickened because of smooth muscle cell proliferation (Figure 3). The right ventricular wall had scattered foci of interstitial fibrosis and degenerate myocytes. Cultures of the pulmonary parenchyma were not done. The pathologic diagnoses were cardiomyopathy and suppurative interstitial pneumonia.

Case 2

A 13-year-old, 68-lb (30.9-kg), spayed female Labrador retriever was presented to the referring veterinarian with a history of gagging, retching, coughing, and respiratory stridor. The dog had been receiving a heartworm preventive, and the most recent antigen test result (obtained 22 months before presentation) had been negative. A thoracic radiographic examination had revealed only small, diffuse pulmonary calcifications. The referring veterinarian had concluded that the dog had chronic bronchitis and laryngeal paralysis. Treatment included enrofloxacin and aminophylline. The dog improved initially but had returned three months later with worsening respiratory signs. An electrocardiographic examination had showed occasional right-ventricular-originating premature beats. Laboratory testing had revealed a low serum thyroxine concentration, so levothyroxine sodium had been added to the therapeutic plan.

Seven months after the initial presentation for the respiratory problem, arytenoid lateralization was performed to alleviate the respiratory obstruction. For 10 days after the surgery, the dog had profound weakness, respiratory stridor, cardiac arrhythmia, and one syncopal episode. Three weeks after the surgery, the dog was referred to the Veterinary Teaching Hospital at Virginia Tech for evaluation of the cardiac arrhythmia. At the time of referral, the dog was being treated orally with levothyroxine (0.016 mg/kg b.i.d.), procainamide (16 mg/kg t.i.d.), theophylline (9.7 mg/kg b.i.d.), dexamethasone (0.008 mg/kg every 48 hours), and carprofen (2.4 mg/kg b.i.d.).

Initial examination, diagnostic tests, and treatment

On physical examination, the dog's rectal temperature was 101.6 F (38.7 C), its pulse rate was 180 beats/min, and its pulse quality was weak. The dog was panting heavily. No heart murmurs or abnormal pulmonary sounds were auscultated. The results of an echocardiographic examination were normal. An electrocardiographic examination revealed occasional right ventricular premature beats. The cardiac silhouette was normal on thoracic radiographs, but there was a mild, diffuse interstitial lung pattern that was considered a secondary complication to respiratory compromise. The radiographs also showed numerous radiopaque, small nodules primarily in the cranial lung lobes that were thought to be age-related calcification. The results of a complete blood count were normal.

Since the clinical signs in this dog were not entirely attributable to the cardiovascular system, a consult from the surgery service was requested to evaluate the laryngeal paralysis and the prior surgery. The dog was anesthetized for a brief period, and visual inspection of the laryngeal area revealed bilateral obstruction and substantial laryngeal and perilaryngeal swelling. The surgical procedure had not successfully reduced the laryngeal obstruction, so a right arytenoid lateralization was performed within 48 hours of presentation to the teaching hospital.


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