Page 265 - Clinical Small Animal Internal Medicine

24 Congenital Heart Disease 233

The degree of shunting depends on the size of the Stenotic Valve Lesions
VetBooks.ir defect and the relative resistance of the pulmonary ver- Subaortic Stenosis
sus the systemic circulation. Typically, flow is driven
Aortic stenosis occurs almost exclusively in the dog and
from the left atrium across the ASD to the right,
thereby increasing blood flow through the lungs. In is very rare in the cat. In almost all cases, obstruction is
the result of subaortic tissue that narrows the left ven-
contrast to left‐to‐right shunts such as PDA and VSD tricular outflow tract. The tissue may be a discrete
that result in left heart enlargement, atrial‐level shunts fibrous ridge or a tunnel‐like narrowing. Rarely, valvar
cause right heart enlargement as the increased pulmo- aortic stenosis is seen with fusion and/or thickening of
nary venous return is shunted to the right atrium. With the valve leaflets. In order to maintain forward stroke
profound shunting, pulmonary hypertension and shunt volume, such that the same volume of blood is pumped
reversal (Eisenmenger’s physiology) may occur. Flow out of the left ventricle with each heartbeat, the blood
across the atrial septum may also develop if right atrial must accelerate through the narrowing at a higher veloc-
pressure becomes elevated, even in the presence of a ity. This requires that a greater left ventricular pressure
normally formed atrial septum. This develops because be generated. The elevated left ventricular pressure leads
the atrial septum is composed of two membranes that to increased left ventricular wall stress and the develop-
are closed during the first week of life as left atrial ment of concentric left ventricular hypertrophy.
pressure exceeds right atrial pressure. If the animal has The natural history of SAS includes a near normal
right‐sided heart disease that elevates right atrial pres- lifespan for patients with mild disease; those with
sure (pulmonary stenosis, tricuspid dysplasia, tetral- moderate to severe disease may experience exercise
ogy of Fallot), then the membranes may remain intolerance, syncope, left‐sided congestive heart failure,
separate and allow flow across the atrial septum or sudden cardiac death. All patients with SAS are
from right to left, referred to as a patent foramen believed to be at higher risk for development of bacterial
ovale (PFO). endocarditis due to damage of aortic valve integrity from
In the setting of a large ASD or concurrent defects,
presenting signs will be an asymptomatic heart murmur, the turbulent, high‐velocity jet. As such, antibiotic
prophylaxis is advised for surgical or dental procedures,
pulmonary overcirculation, or weakness, lethargy, or or in cases of potential bacteremia (e.g., skin laceration).
cyanosis associated with pulmonary hypertension and Screening young dogs for SAS bears some mention.
shunt reversal.
First, SAS may progress as the dog grows because the
subvalvar ridge does not change in size while the heart
Atrioventricular Septal Defects and stroke volume increase with the patient’s develop-
Defects of the atrioventricular septum (AVSD) may be ment. Therefore, the final assessment of severity can
considered separate from ASD or VSD. The atrioven- only be made when the patient is full grown or nearly so.
tricular septum is composed of centrally located tissue Second, screening breeding dogs for mild disease is a
derived from the endocardial cushions. With an AVSD, very real clinical problem as some breeds (boxer, grey-
defects may occur in the interatrial septum above the hound, etc.) have aortic flow velocities that, with excite-
atrioventricular valves (a primum defect) or the inter- ment, may be considered mild stenosis. This creates a
ventricular septum just below the atrioventricular gray zone between normal and mildly affected that can
valves (inlet VSD), and may cause concurrent malfor- make breeding recommendations challenging.
mations of the atrioventricular valves. These defects
were formerly referred to as endocardial cushion
defects or defects in the atrioventricular canal. Signs Pulmonary Valve Stenosis
vary depending on the relative size of each defect, Pulmonary valve stenosis (PS) is principally a disease of
but both congestive heart failure and cyanosis are the valve leaflets and/or annulus, rather than the subval-
common. AVSDs are relatively uncommon in dogs, var region as in SAS. PS comes in varying forms – fusion
but are seen in roughly 10% of cats with CHD. of the valve leaflets resulting in a narrowed orifice and
The diagnosis is made by demonstration of the atrio- doming valves, valvular thickening and dysplasia result-
ventricular valves in the same imaging plane and vari- ing in thick immobile valves that do not open normally,
ably sized defects in the ventral interatrial septum, and annular hypoplasia where the valve annulus is abnor-
inlet interventricular septum, and septal leaflets of the mally small. The same hemodynamic derangements
atrioventricular valves. There are also partial forms of described above for SAS apply to the right ventricle in
AVSD recognized, depending on the presence/absence patients with PS. Right ventricular concentric hypertro-
of atrial and ventricular septal defects as well as phy is common and at times can be so severe as to create
the degree of development of distinct mitral and tri- a dynamic and muscular subvalvar obstruction. In these
cuspid annuli. instances, the right ventricle (RV) hypertrophies to such