The primary objectives of the cardiovascular evaluation for animals with congenital heart disease are to define the nature
and severity of the anatomic defect present. Familiarity with the available therapeutic options, their efficacy and limitations
is necessary before an accurate prognosis can be offered to the owner.
Acyanotic congenital heart defects: left to right shunts
The normal circulation is anatomically and functionally separated into two sides. The right side (systemic veins, right atrium,
right ventricle and pulmonary arteries) is a low-pressure circuit while the left side (pulmonary veins, left atrium, left
ventricle, and systemic arteries) is a high-pressure circuit. The direction and magnitude of blood flow across any abnormal
communication is dependent on: 1) The size of the communication and 2) the relative pressure difference between the communication.
Patent ductus arteriosus (PDA) including right to left shunting lesions
In the fetus the ductus arteriosus serves to shunt the majority of the right ventricular output away from the non-functioning
lungs. Expansion of the lungs, increased oxygen concentrations and removal of the umbilical circulation at the time of birth
promotes ductal closure along with a marked decline in the pulmonary vascular resistance. Failure of ductal closure usually
results in a left to right shunt from the descending aorta to the pulmonary artery with an excess volume load placed on the
pulmonary arteries and veins, left atrium, left ventricle and aortic arch. The size of the shunt depends on the internal diameter
and length of the ductus arteriosus. The ductus is usually funnel-shaped with the aortic end wider than the pulmonary arterial
end. Histology of the patent ductus reveals a wall structure resembling that of the aorta rather than that of a normal ductus.
In the presence of a very large, wide PDA the magnitude and direction of shunted blood is determined by the relative resistance
of the pulmonary and systemic circulations. In these dogs the elevated pulmonary vascular resistance present at birth does
not fall normally and results in right to left shunting or bidirectional shunting. On rare occasion pulmonary hypertension
develops later in life thereby truly reversing the direction of the shunt (Eisenmenger's physiology).
• Historically the most common congenital heart defect in dogs although the recent popularity of large breed dogs has
resulted in increased prevalence of SAS. PDA is much less common in cats.
• Females are over-represented.
• Physical examination findings include:
· A continuous "machinery" murmur that is heard best at the left heart base. The continuous murmur may be confined
to the heart base while a systolic murmur of mitral insufficiency is ausculted over the left apical region.
· Bounding (or waterhammer) pulses are frequently identified because of the increased systolic and decreased
diastolic aortic pressures (widened pulse pressure).
· Common clinical signs include stunted growth or evidence of left sided heart failure (dyspnea, tachypnea,
coughing, exercise intolerance.)
· PDA with pulmonary hypertension has no murmur but may have a split S2, differential cyanosis, and hindleg weakness.
These dogs often display "differential cyanosis" where the hindlimbs are affected while the forelimbs are normal. This develops
because of the communication of the pulmonary artery with the descending aorta.
• Electrocardiographic findings
· Variable but often marked left ventricular enlargement pattern, possible left atrial enlargement and secondary
ST segment changes associated with hypoxia.
· Advanced cases may show supraventricular tachyarrhythmias (APCs, A fib) or less frequently ventricular arrhythmias.
· A right ventricular enlargement pattern is almost always evident in cases of right to left shunting with pulmonary
• Thoracic radiography
· Enlargement of the left atrium, left ventricle, aortic arch, main pulmonary artery along with pulmonary vascular
overcirculation (enlargement of both pulmonary arteries and veins).
· Evidence of left sided heart failure may be present.
· Dogs with right to left shunting often display pulmonary vascular undercirculation (hypovascularity of pulmonary
arteries and veins), a prominent right heart pattern, dilation of the main pulmonary artery and localized dilation of the
• Echocardiography: Serves to evaluate the severity of volume overload as reflected by changes in the left heart chamber
dimensions, detect other coexisting congenital heart defects, and assess myocardial function.
· In dogs with left to right shunts the prognosis is excellent with surgical or transcatheter closure of the defect
prior to the development of left-sided heart failure. Without correction puppies with large shunts may die before four weeks
of age, dogs with intermediate sized shunts may live for several years although the majority will be dead by 2 years of age.
Dogs with small shunts (uncommon) may live normal lives.
· In dogs with right to left shunts the prognosis is guarded. Some dogs may survive for long periods of time with
exercise restriction and periodic phlebotomy or agents utilized to decrease red blood cell production.
• Treatment: Ideally involves surgical correction of left to right shunts via thoracotomy or less invasive embolization
procedures prior to the development of clinical signs. In cases of left to right shunts with congestive heart failure stabilization
is achieved with standard medical therapy followed by closure. Surgery is contraindicated in dogs with right to left PDAs
and instead efforts are aimed at preventing hyperviscosity via periodic phlebotomy.