Page 139 - Small Animal Internal Medicine, 6th Edition

CHAPTER 5 Congenital Cardiac Disease 111

peak shunt flow velocity is used to estimate the systolic ATRIAL SEPTAL DEFECT
pressure gradient between the LV and RV. Small (restric- Etiology and Pathophysiology
VetBooks.ir tive) VSDs cause a high-velocity shunt flow (≈4.5-5 m/sec) Several types of ASD exist. Those located in the region of the
because of the normally large systolic pressure difference
fossa ovalis (ostium secundum defects) are more common
between the ventricles. Lower peak shunt velocity (nonre-
strictive VSD) implies increased RV systolic pressure, either in dogs. An ASD in the lower interatrial septum (ostium
from PS or pulmonary hypertension. Left heart dilation is primum defect) is likely to be part of the AV septal (endo-
evident when the shunt is large; RV dilation occurs uncom- cardial cushion or common AV canal) defect complex,
monly as most VSDs are located high in the interventricular especially in cats. Other ASD locations (sinus venosus or
septum with blood shunting nearly immediately into the coronary sinus defects) are rare. Animals with ASD com-
RV outflow tract. Echocardiography should be repeated monly have other cardiac malformations as well. In most
when patients reach adult size (usually approximately 1 year cases of ASD, blood shunts from the LA to RA and results
of age). in a volume overload to both the right heart and pulmo-
Cardiac catheterization, oximetry, and angiocardiogra- nary circulation. However, if PS or pulmonary hypertension
phy uncommonly are performed clinically but can allow is present, right-to-left shunting and cyanosis can occur.
measurement of intracardiac pressures, indicate the presence Patent foramen ovale, where embryonic atrial septation
of an oxygen step-up at the level of the RV outflow tract, and has occurred normally but the overlap between the septum
show the pathway of abnormal blood flow. primum and septum secundum does not seal closed, is not
considered a “true” ASD, but is a common cause of right-to-
Treatment and Prognosis left shunting in the presence of abnormally high RA pressure
Small restrictive VSDs (less than 40% of aortic diameter, (as in PS or pulmonary hypertension).
shunt velocity greater than 4.5 m/s) have an excellent prog-
nosis; animals typically live a normal life span with no treat- Clinical Features
ment required. There are sporadic reports of spontaneous The clinical history in animals with an ASD is usually non-
VSD closure within the first 2 years of life, either from myo- specific. Physical examination findings associated with an
cardial hypertrophy around the VSD or a seal formed by the isolated ASD often are unremarkable. Because the pres-
septal tricuspid leaflet or a prolapsed aortic leaflet. Animals sure difference between right and left atria is minimal, no
with large nonrestrictive VDSs (greater than 60% of aortic murmur is expected across the ASD, although large left-
diameter, shunt velocity less than 4.0 m/s) have a more to-right shunts can cause a murmur of relative PS. Fixed
guarded prognosis; left-sided CHF is the most common splitting (i.e., with no respiratory variation) of the second
outcome, although in some cases pulmonary hypertension heart sound (S 2 ) is the classic auscultatory finding, caused
with shunt reversal develops instead. Animals that develop by delayed pulmonic and early aortic valve closures. Rarely,
clinical complications related to a large VSD typically display a soft diastolic murmur of relative tricuspid stenosis might
clinical signs at an early age. In a large retrospective case be audible. Large ASDs can lead to signs of right-sided or
series of VSDs in dogs and cats, the vast majority of patients biventricular CHF.
with VSDs (81%) were asymptomatic at time of diagnosis
and remained asymptomatic throughout an average 12-year Diagnosis
life span. Right heart enlargement, with or without pulmonary trunk
For asymptomatic patients with a small restrictive VSD, dilation, is found radiographically in patients with large shunt
no treatment is indicated. For patients with a larger nonre- volumes (see Table 5.2). Pulmonary overcirculation can be
strictive VSD, left-sided CHF is managed medically when apparent unless pulmonary hypertension has developed. Left
and if it occurs. Definitive therapy for large nonrestric- heart enlargement is not generally evident unless another
tive VSDs generally requires cardiopulmonary bypass for defect such as mitral insufficiency is present. The ECG can
open-heart surgery (patch grafting). Transcatheter delivery be normal or show evidence of RV and RA enlargement.
of an occlusion device can be successful in medium- to Echocardiography is likely to show RA and RV dilation,
large-breed dogs with muscular VSDs; other VSD loca- with or without paradoxical interventricular septal motion;
tions generally are less amenable to interventional closure larger ASDs can be visualized. Care must be taken not to
due to proximity of the defect to the aortic or pulmonic confuse the thinner fossa ovalis region of the interatrial
valve. Historically, large left-to-right shunts sometimes have septum with an ASD, because echo dropout also occurs here.
been palliated by surgically placing a constrictive band Doppler echocardiography can allow identification of smaller
around the pulmonary trunk to create a mild supraval- shunts that cannot be clearly visualized on 2-D examination,
vular PS. This raises RV systolic pressure in response to but venous inflow streams can complicate this. An agitated
the increased outflow resistance, decreasing shunt volume saline contrast study can be used to identify right-to-left
from the LV to RV. However, an excessively tight band shunting ASDs. Although rarely performed clinically, cardiac
can cause right-to-left shunting (functionally analogous catheterization shows an oxygen step-up at the level of the
to a T of F). Palliative surgery should not be attempted right atrium (RA). Abnormal flow through the shunt might
in the presence of pulmonary hypertension and shunt be evident after the injection of contrast material into the
reversal. pulmonary artery.