Missy's echo results
- Diagnosis: Congenital heart disease. Missy has a large atrial septal
defect/ventricular septal defect (8 mm) a hole in the lower atrial
septal and upper ventricular septal wall where the chambers join which
allows blood to shunt right to left and left to right in the heart.
Her heart chambers are dialated and her pulmonary artery and veins are
dilated. Her right ventricular wall is mildly thickened. The defects
can lead to congenital heart disease (CHF) with fluid retention in the
lungs, chest cavity and/or abdomen. Therefore I would recommend
starting her on a low dose of furosemide.
She called in a prescription of furosemide 10 mg/ml .3 mg once daily.
The compounding pharmacy here says that can't be compounded
transdermally because the molecule is too large.
Comments? Is this as bad as it sounds to me?
I am sorry that Missy's echo showed this kind of heart
defect. There are few kitties and owners here who are
dealing with VSD, although I don't recall off-hand any
mentions of ASD or both. I am unfamiliar with the
treatment of this heart defect.
You mentioned that the vet "called in a prescription
of furosemide 10 mg/ml .3 mg once daily."
A oral dose of 0.3 mg furosemide would be impossibly
small to give as a pill. In the liquid form you
describe, that would be an oral dose of only 30
microliters (0.03 ml) from a 10 mg/ml solution. You
can measure an amount that small with a "tuberculin"
syringe. I would double check the dosage with the vet
and the pharmacy and make sure to get a syringe that
can measure that kind of small volume. It would be
easier to measure accurately if the solution were more
dilute than that, for example a 1 mg/ml soultion.
Then you would give 0.3 ml which might be more
I've included a bit more info below my signature
Here are some links that might help you get started :
First a link to a short article that might be useful:
and from a meeting proceeding
ATRIAL SEPTAL DEFECTS (ASD)
ASD are uncommon congenital heart defects in small
animals. They can appear as an isolated defect or they
may be part of a complex malformation. Four types of
ASD have been described: 1) ostium secundum, involving
the region of the fossa ovalis; 2) ostium primum or
partial atrioventricular canal defect, located in the
lowermost portion of the interatrial septum and
associated with endocardial cushion defects; 3) sinus
venosus involving the superior portion of the
interatrial septum; 4) coronary sinus, located in the
posteroinferior angle of the atrial septum.
Small ASD are not usually hemodynamically significant.
Because the pressures between the two atria are
similar, the shunt flow across an ASD does not
generate murmur, but a murmur of relative pulmonic
stenosis may be detected. Only right heart failure
develops in severe cases.
VENTRICULAR SEPTAL DEFECTS (VSD)
Depending on the location, VSD are classified as: a)
membranous/perimembranous, the most common type in
dogs, b) outflow (infundibular/supracristal), c)
inflow (atrioventricular canal), and d) muscular
(trabecular). VSD can appear as isolated lesion or in
association con others heart defects (i.e., PS,
pulmonary atresia, truncus arteriosus and
double-outlet right ventricle). Some defects can
predispose to prolapse of the aortic valve into the
Pathophysiology: The physiologic consequences of a VSD
are determined by the size of the defect and the
relative resistance in the systemic and pulmonary
vascular beds. If the defect is small ("restrictive"
VSD), there is little or no functional disturbance,
since pulmonary blood flow is increased only
minimally. In contrast, if the defect is large ("non
restrictive" VSD), the ventricular systolic pressures
are equal and the magnitude of flow to the pulmonary
and systemic circulation is determined by the
resistances of the two beds. Initially, systemic
vascular resistance excess pulmonary vascular
resistance, so that left-to-right shunting
predominates. As pulmonary flow increases, there is
increased venous return to the left atrium and left
ventricle, and the left ventricular diastolic pressure
can increase. Left ventricular failure is likely when
the left-to-right shunt is great. Over the time, the
pulmonary vascular resistance usually increases, and
the magnitude of left-to-right shunting declines. If
the pulmonary vascular resistance equals or exceeds
the systemic resistance the shunting of blood from
left to right then ceases, and right-to-left shunting
Breed predispositions: English bulldog, Keeshond
(genetic basis documented), English springer spaniel
and Beagle are predisposed.
Clinical assessment: Most animals that have survived
through the first months without clinical signs, can
tolerate the defect for many years without clinical
signs. A harsh, holosystolic murmur, audible maximally
over the ventral right thorax, often near to the
sternum is present. Murmurs of the relative pulmonic
stenosis or aortic regurgitation (prolapse of the
aortic valve into the defect) may be audible with VSD.
Thoracic radiographic findings in dogs with VSD are
variable, but usually left atrial and ventricular
dilation, pulmonary overcirculation, a dilated main
pulmonary artery, and variable degrees of right
ventricular enlargement are present. The ECG may show
evidence of left, right or biventricular enlargement,
depending on hemodynamic consequences of the shunt.
Echocardiography is useful to confirm the diagnosis of
a VSD and to help assess the severity of the defect.
Spectral Doppler shows a high velocity jet (Vmax > 4.5
m/sec) thorough a restrictive VSD and increased peak
pulmonary artery velocity owing left-to right shunt.
Clinical management: Definitive treatment of
symptomatic or severe lesions requires surgery using
cardiopulmonary bypass and is rarely performed.
Pulmonary artery banding can be used to create
supravalvular pulmonary stenosis and decrease the
magnitude of left-to-right shunting in dogs with large
VSD. If surgical correction or palliation is not an
option, medical management of congestive heart failure
may be required. Prophylactic antibiotic therapy
should be considered in patients with VSD when there
is known potential for hematogenous exposure to
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- Kelley, this was meant for you . . .
My kitty has a cardiac cushion defect which covers the atrium and
ventricle and means all her four chambers are in contact with each
other. She is on Fortekor at 2.5mg each morning as she is only 6 months
old. Her brothers all have a similar defect but not as bad.
It sounds very similar to your kitty. My Milli is coping quite well and
eating and playing like the others, although she often gets breathless.
She was on furosimide but they took it off her as her lungs aren't
congested. I also use the carnitine, co-Q supplements and this helped a
My Lilly has VSD, with thickening secondary to that defect. Her foster mom,
Moriah took her to OSU where she was started on enalapril and a low dose of
Lilly is asymptomatic at this stage and the lasix was simply to prevent any
fluid build up which *might* happen. I took her off this because I don't
think (and my vet agrees) that prophylactic lasix is going to do any good at
all. Cats, like humans, can develop a resistance to lasix over time,
requiring higher and higher doses to be effective and frankly, if the cat is
not in congestive heart failure (has no fluid in or around the lungs) it
doesn't need lasix. Regular vet care, careful monitoring of breathing and
behavior patterns will be enough to know when/if the cat will need
Aside from that, CHF is a catastrophic event in the sense that there's no
such thing as having a little CHF. It happens when the disease has
progressed to the point where there's a pathological pressure differential
in the lungs, causing fluid to seep from the vessels and into the lung
tissues. It's *not* something like humans taking low-dose aspirin to help
prevent heart disease -- low dose lasix will *not* prevent CHF, all it is
likely to do in the best possible scenario is delaying the symptoms of CHF
from showing up by a matter of an hour or two. If and when CHF occurs it
requires higher doses of lasix, possibly a second diuretic, and
cardiac-specific drugs to counteract.
I'm all for meds if they are going to help, but I think you may want to
discuss this with your vet. Lilly is getting enalapril to help regulate her
heart which is more likely to prevent fluid build up in the first place. As
for how bad it sounds ... it's hard to say. Lilly, aside from a REALLY LOUD
murmur has no outward signs on the disease and acts like any other cat.
Some cats go for years with these defects, others don't and it's hard to say
what will happen to any individual cat.
The important thing is that you know what you're up against now and can do
whatever you can to help Missy. A high-quality diet, supplements, and
appropriate meds can all give her the best chance possible to live well and
hopefully longer. As for the lasix -- if you're not comfortable going
against your vet's advice right now, it will not hurt her short-term to get
a low dose until you've had time to research this for yourself and decide
what course of action you want to take. I'd suggest you look into
enalapril. Enalapril, in this instance, is used as a "afterload reducer"
and decreases left-to-right shunting and improves overall systemic blood
flow and is recommended for both atrial and septal defects.
Another issue you'll need to address is clot prevention -- all heart kitties
are susceptible to forming clots, which can be life-threatening. There are
different options for this, such as aspirin therapy (dubious benefits), low
molecular weight heparins, plavix, and supplements such as nattokinase (an
enzyme that 'eats' clots, Lilly gets this). Our septal defect kitties are
even more a risk for these clots, so addressing this is something you can do
that has a real chance at helping to prolong and improve Missy's life.
I hope all this helps ... I know it's a lot of information and you're new to
this. It can all be a little overwhelming at first!
On 2/1/07, Kelley <moonvine@...> wrote:
> Diagnosis: Congenital heart disease. Missy has a large atrial septal
> defect/ventricular septal defect (8 mm) a hole in the lower atrial
> septal and upper ventricular septal wall where the chambers join which
> allows blood to shunt right to left and left to right in the heart.
> Her heart chambers are dialated and her pulmonary artery and veins are
> dilated. Her right ventricular wall is mildly thickened. The defects
> can lead to congenital heart disease (CHF) with fluid retention in the
> lungs, chest cavity and/or abdomen. Therefore I would recommend
> starting her on a low dose of furosemide.
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