Share it:

section content

  • A 1-year-old male castrated German Shepherd Dog presented to Inland Empire Veterinary Imaging for an echocardiogram to evaluate for an underlying cause of collapse episodes with excessive panting when excited that had developed in the last couple of months. These episodes had increased in frequency and he became wobbly multiple times a day. His legs would start shaking and he’d have to lay down. Primarily his back legs would shake and he couldn’t hold himself up.
  • The patient had no prior history of a heart murmur or arrhythmia or previous exercise intolerance.
  • The physical exam on presentation was unremarkable.
  • Thorax radiograph from the rDVM revealed concern for mild right-sided heart enlargement.


LLAT thoracic radiographcaption
RLAT thoracic radiographcaption
DV thoracic radiographcaption
VD thoracic radiographcaption
1 / 4
  • Eccentric and concentric right ventricular enlargement, both. Eccentric hypertrophy of the right atrium. There was interventricular septal wall flattening.
  • There was severe tricuspid valve regurgitation (5.57 m/s; reference range <2.25 m/s and pressure gradient of 124.12 mmHg; reference range <38 mmHg) with mild tricuspid valve thickening.
  • There was no evidence of mitral, aortic, or pulmonic valve thickening/abnormalities or regurgitation.
  • There was no evidence of atrial or ventricular septal defects.
  • The remaining cardiac measurements were normal.

Thorax radiographs from the rDVM were also reviewed, revealing generalized cardiomegaly with an aortic aneurysmal bulge, pulmonary arterial and venous over circulation, and mild, diffuse bronchial pulmonary pattern.

Given the radiographic changes in the thorax, the high-pressure gradient of tricuspid valve regurgitation, and the lack of detectable changes to explain the right ventricular eccentric and concentric hypertrophy (i.e. no pulmonic stenosis), a bubble test of the abdominal aorta was performed to assess for the presence of a right-to-left shunt (reverse PDA).


Agitated saline was injected into a 20 gauge catheter in the right cephalic vein while a 3-10 MHz curvilinear ultrasound probe was positioned over the mid-abdominal aorta and caudal vena cava. The test was positive with gas bubbles evident within the aorta within 10 seconds of the cephalic vein injection gradually clearing followed by a significant delay prior to gas bubbles being visualized within the caudal vena cava.

Imaging Diagnosis:

  • Based on a right-to-left shunting with right ventricular/atrial eccentric hypertrophy, right ventricular concentric hypertrophy, tricuspid valve regurgitation, and evidence of severe pulmonary hypertension with no additional cardiac anomalies a reverse patent ductus arteriosus (PDA) was diagnosed.

No treatment was recommended at this time as patients with a reverse PDA are not surgical candidates. Consultation with a veterinary cardiologist was recommended to discuss whether or not a phosphodiesterase inhibitor (i.e. Sildenafil) would be recommended. Exercise restriction was discussed as a recommendation with the rDVM.

Patent ductus arteriosus (PDA) is one of the most common congenital cardiac anomalies in dogs with many breeds reportedly affected, including German Shepherds. PDAs have a known hereditary component.

The ductus arteriosus is a normal in-utero muscular vascular structure that allows blood flow between the aorta and the main pulmonary artery. In the fetus, the ductus arteriosus allows blood to bypass the non-aerated lungs in-utero. Normal atelectic fetal lung results in pulmonary arterial pressure exceeding aortic pressures and a “normal” right to left shunt. Normally, the fetus takes its first few breaths at birth, expanding the lungs and resulting in a marked decrease in pulmonary vascular resistance secondary to increased oxygenation. This stimulates muscular constriction and functional closure within minutes and eventual complete structural closure of the ductus arteriosus within ~1 month.

In normal animals, once the ductus arteriosus closes, there is a gradual decrease in pulmonary arterial resistance. In the fetus, the medial layer of the pulmonary artery smooth muscle is increased. As ventilation begins, hypoxic vasoconstriction of the pulmonary arterial resistance decreases, and the medial layer gradually thins to reach the normal adult thickness. In normal adults, the pulmonary arterial vascular resistance is expected to be one-fifth that of the systemic vascular resistance.

Patent ductus arteriosus occurs when the ductus does not close. In conjunction with the higher systemic and left ventricular pressure, this allows continued blood flow to shunt from the aorta to the main pulmonary artery (left to right) resulting in the characteristic machinery murmur.

The process explained above, in which normal dogs have a gradual decrease in pulmonary arterial resistance, is delayed in patients with PDA due to the left to right shunting and subsequently increased pulmonary blood flow. In these patients, there is a persistent increase in pulmonary vascular resistance likely due to vestigial medial hypertrophy and vasoconstriction. This increased pulmonary arterial pressure and blood flow leads to over circulation of the pulmonary parenchyma and ultimately results in severe pulmonary arterial hypertension. As pulmonary arterial pressure increases, the right side of the heart works harder to compensate leading to right-sided hypertrophy.

Eventually, this increased pressure stimulates a pathological response in the pulmonary arteries. While the mechanism is not known, the most likely explanation involves injury to the endothelial cells causing the release of growth factors that stimulate medial smooth muscle hypertrophy and intimal hyperplasia. The pulmonary arteries have narrowed lumens resulting in increased vascular resistance. This causes gradual equilibration of pressure within the pulmonary and systemic vasculature. Once equalized there is a loss of turbulent blood flow, thus, any auscultable heart murmur. Once the pulmonary vascular resistance exceeds that of the systemic vascular resistance, the blood flow reverses (right to left shunt). –

There are now large volumes of deoxygenated blood shunting to the systemic circulation resulting in caudal cyanosis, weakness, exercise intolerance, and collapse. This cycle continues and ultimately in later stages, due to chronic hypoxia and decreased renal blood flow, there is secondary polycythemia. Patients are treated supportively to address any presenting clinical signs with most dogs not living past 5-6 years of age.


  • Chetboul, V., Bussadori, C., and de Madron, E. (2016). Clinical Echocardiography of the Dog and Cat (E. du Madron). Elsevier.
  • Kittleson, M. D. and Kienle, R. D. (1998). Small Animal Cardiovascular Medicine. Mosby.
  • Penninck, D., d’Anjou, M.-A., Mellor, B., & d’Anjou, M.-A. (2015). Atlas of small animal ultrasonography. John Wiley & Sons Incorporated.