A Ventricular Septal Defect (VSD) is a congenital cardiac disease, causing communication between the left and right ventricle.
These can occur in numerous locations and the changes to be expected depends on the exact location.
The development of left-sided (most common in veterinary medicine) or right-sided congestive heart failure is possible.
Based on the precise findings, we will discuss appropriate management options.
Some cases require monitoring, others medical management, and some surgical intervention
Congenital Mitral Valve Dysplasia is a condition where the mitral valve (separating the left atrium and left ventricle) did not form correctly at birth. As a result, the valve does not close (coapt) normally.
This poor coaptation allows reverse blood flow (left ventricle into left atrium), which is termed regurgitation or insufficiency.
This disease is progressive in that the chambers will continue to dilate, but the valve structure likely will not change.
Routine rechecks are required to monitor for any changes to the left atrium or ventricle that may warrant additional testing or direct medical management of this disease.
Eventually, this disease can lead to the development of congestive heart failure (fluid in the lungs), which is a medical emergency that makes breathing very difficult.
A right to left Patent Ductus Arteriosus (Reversed PDA or rPDA) is a congenital defect where the ductus arteriosus (fetal vascular connection) remains present after birth.
The pulmonary pressures rise dramatically due to a problem within the lungs (Eisenmenger’s Physiology), causing blood to flow from the main pulmonary artery into the descending aorta.
This high concentration of deoxygenated blood causes a high degree of deoxygenated blood to flow to the back half of the body, particularly the kidneys.
This is seen clinically as differential cyanosis (blue/purple caudal membranes, pink cranial membranes). A rPDA results in severe elevations of the hematocrit (PCV or HCT) as the kidneys respond to the deoxygenated blood by signaling for more red blood cell production.
Affected patients will typically become neurologic (seizures, altered mentation, weakness, collapse, inappetance, or trembling) as the hematocrit rises.
These patients are also at risk for sudden death due to arrhythmias, neurologic conditions (embolic events or seizures), or potentially right-sided congestive heart failure.
There is no cure for this condition.
Therapy is directed towards lowering the pulmonary pressures, thus reducing the degree of shunting and therapeutic phlebotomy (blood draws) as necessary to maintain the hematocrit around 60-65%.
The prognosis is typically poor; however, some patients will live for many years with optimal medical management.
A Patent Ductus Arteriosus (PDA) is a congenital defect where the ductus arteriosus (fetal vascular connection) remains patent after birth.
This allows blood to flow from the aorta into the main pulmonary artery.
If left untreated, this allows severe fluid overload to the left side of the heart.
This causes severe left atrial and left ventricular dilation, eventually resulting in left-sided congestive heart failure (fluid on the lungs).
Affected patients will typically progress into congestive heart failure by 1 year of age and most patients will die by 3 years of age.
It is important to monitor these patients for the development of congestive heart failure as medications are required to control this condition and maximize life expectancy and quality of life. Fortunately, with surgical correction, the life expectancy of patients with this condition is generally normal (unless advanced myocardial insult has happened before diagnosis).
he surgical procedure typically recommended is a transvenous occlusion, but the size of your pet may impact surgical options.
This is a minimally invasive surgery that is performed through a small incision in the rear limb.
The catheter is passed across the PDA from the femoral artery and a device (coil, plug, or occluder) is placed within the PDA.
This allows a blot clot to form that is eventually replaced with fibrous tissue, resulting in a permanent occlusion.