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.


Initial examination and diagnostic tests

2A. A left caudal parasternal long-axis view showing the enlarged right ventricle (RV) and right atrium (RA) of the dog in Case 1 (AO = aorta).
The dog was presented to Virginia Tech five days after the examination by the referring veterinarian. The initial examination revealed weakness, stress-induced cyanosis, and labored breathing. The dog's rectal temperature was 101.3 F (38.5 C), its heart rate was 140 beats/min, and its respiration rate was 70 breaths/min. A grade II/VI systolic murmur was heard over the tricuspid valve area. The lung sounds were harsh and at times were suggestive of a pleural friction rub. An electrocardiographic examination indicated mild right axis deviation. Thoracic radiographs showed right heart enlargement, main pulmonary artery enlargement, and a mild, diffuse interstitial pattern. Repeated pulse oximetry readings averaged 55%. No abnormalities were seen on abdominal ultrasonographic examination. A complete blood count revealed a stress leukogram; the total white blood cell count was 25.8 103 /l (normal = 4.6 to 17.8 103 /l), with 22.962 103 /l segmented neutrophils (normal = 2.8 to 12.8 103 /l), 0.774 103 /l band neutrophils (normal = 0), 0.516 103 /l lymphocytes (normal = 1 to 3.7 103 /l), and 1.548 103 /l monocytes (normal = 0.09 to 0.9 103 /l). Abnormal serum chemistry profile results were elevated blood urea nitrogen (57 mg/dl; normal = 8 to 27 mg/dl) and creatinine (1.8 mg/dl, normal = 0.6 to 1.4 mg/dl) concentrations. The dog's urine specific gravity was 1.008.

Echocardiographic examination

2B. The same view as in Figure 2A but with color Doppler applied to the two-dimensional image. The green reflects the substantial tricuspid regurgitation during ventricular systole. This view allows for good alignment between the regurgitant jet and the Doppler beam, providing an accurate assessment of jet velocity.
An echocardiographic examination revealed a right ventricle that was grossly dilated and appeared larger than the left ventricle. The right ventricular free wall was thick (0.6 cm) compared with the left ventricular free wall (0.9 cm), suggesting that this dog had right ventricular hypertrophy. The increased pressure or volume in the right ventricle displaced the interventricular septum to the left, making the septum appear flattened. The displacement of the septum as well as the potentially decreased blood flow to the left side of the heart due to reduced pulmonary blood flow resulted in a left ventricle that was smaller than expected. The M-mode values from the right short-axis view showed a left ventricular diastolic diameter of 2.14 cm (normal = 3.4 cm) and left ventricular systolic diameter of 1.43 cm (normal = 2.1 cm) (Figure 1). Substantial tricuspid regurgitation could be seen from several imaging planes (Figures 2A & 2B).

2C. This continuous wave Doppler profile was made from an image similar to that displayed in Figure 2B. The scale to the left reveals that the peak right atrial jet velocity was between 4.5 and 5 m/s. With the modified Bernoulli equation, this translates to a systolic pressure gradient of 81 to 100 mm Hg (normal = 20 to 25 mm Hg) and suggests that the peak systolic right ventricular and pulmonary artery pressure was at least 81 mm Hg.
Continuous wave Doppler echocardiography was used to measure the velocity of the tricuspid regurgitant jet from the left caudal parasternal window (Figure 2B). This view allowed excellent Doppler alignment ( 20 degrees) with the jet so that the flow profile was an accurate representation of the blood velocity between the right ventricle and the right atrium. The velocity of the jet consistently ranged between 4.5 and 5 m/s (Figure 2C). Using the modified Bernoulli equation (P = 4V2 ) to convert the peak velocity of the regurgitant jet to a pressure (P = pressure gradient in mm Hg; V2 = peak velocity distal to an orifice or obstruction), we estimated that the range was 81 to 100 mm Hg (normal = 20 to 25 mm Hg) before adding an estimated right atrial pressure (6 mm Hg). So the peak systolic pressure in the right ventricle and pulmonary arterial system ranged from 87 to 106 mm Hg. We eliminated pulmonic stenosis as a cause of the right ventricular hypertension by evaluating the right ventricular outflow tract and pulmonary valve region. A pulmonary regurgitant jet could not be identified, so it was not possible to estimate the diastolic pressure in the pulmonary artery.


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