This cardiac defect occurs in all animals, but is more likely to be diagnosed in the young.
The condition is the persistence of the ductus arteriosus after birth. During fetal life, the ductus arteriosus connects the pulmonary artery to the descending aorta. This fetal vessel allows most of the blood to bypass the developing lungs and go directly to the aorta and systemic circulation. In fetal life oxygen is provided by the placenta while the lungs are developing. At birth, the animal takes a breath of air and uses its lungs for the first time. High levels of oxygen from the pulmonary vasculature enter the circulation and the ductus arteriosus responds by contracting the smooth muscles lining its vessel wall. The functional closure of the ductus arteriosus occurs within 2-3 days after birth and with time it will become an anatomical closure.
However, some animals have a ductus arteriosus that doesn't respond to the increased oxygen at birth and remains open (patent). After birth PDA causes a reversal of blood flow from the higher pressure of the descending aorta through the ductus arteriosus to the pulmonary artery and into the lungs. This is known as left-to-right shunting. The shunting of blood in this manner overwhelms the pulmonary vasculature and the left side of the heart. The increased volume of blood from the lungs travels to the left atrium and left ventricle which respond to the added pressure by dilation and hypertrophy.
As a result, PDA can eventually lead to pulmonary oedema and left-sided congestive heart failure. Normally the pulmonary circulation is equipped to handle increased volumes of blood without pulmonary arterial pressure changes. However, sometimes the increased blood volume in the lungs causes gross changes to the pulmonary arterioles causing pulmonary hypertension and raised pulmonary arterial pressures. If the pressure is high enough, it can cause a reverse PDA (right-to-left shunt) and unoxygenated blood will bypass the lungs heading straight for the descending aorta and the systemic circulation.
Clinical signs include left sided congestive heart failure, exercise intolerance, differential cyanosis (reverse PDA) and hindlimb weakness (reverse PDA). Sometimes, depending on severity of defect, there may be no clinical signs.
It is a very common condition in dogs. Predisposed breeds include toy breeds (Yorkshire Terrier, Pomeranian, Maltese, Toy Poodles); Miniature Poodles, Shetland Sheepdogs, German Shepherds, *Collies. There has been found to be a greater occurrence in females.