VSD?

Sonopath Forum

– 13 month old MN Savannah cat with a grade 3-4 continous heart murmur

– echo was tough on this one! – hard to get really clear images but I am suspicious of a VSD

– it looks like the flow through the VSD is bi-directional?

– I could not get a TR jet to look for pulmonary hypertension but to me the  IVS looks a little flattened so I am suspicious

– the LA is normal , PA Max vel 1.53 m/s, Ao Max Vel  0.90m/s  , no AI

– as far as I know the cat has been asymptomatic and last bloodwork did not show an elevated PCV

– 13 month old MN Savannah cat with a grade 3-4 continous heart murmur

– echo was tough on this one! – hard to get really clear images but I am suspicious of a VSD

– it looks like the flow through the VSD is bi-directional?

– I could not get a TR jet to look for pulmonary hypertension but to me the  IVS looks a little flattened so I am suspicious

– the LA is normal , PA Max vel 1.53 m/s, Ao Max Vel  0.90m/s  , no AI

– as far as I know the cat has been asymptomatic and last bloodwork did not show an elevated PCV

A couple of questions:

1. VSD for sure?

2. Does this look severe – I have read that the max  velocity of the defect should be aorund 5 m/s but I am getting readings lower than this (consistently) so does this indicate a lower pressure gradient and thus more risk of reverse shunting?

3. If there is bi-directional flow, does this not indiacte that some reverse shunting is occuring

Sorry if these questions appear a bit dumb, but I haven’t found a good resource to read about VSD’s in cats

 

Comments

EL

Yes nice clean vsd jacquie!

Yes nice clean vsd jacquie! bidirectional. this is the most common congenital lesion in cats but looks compensated at the moment.

EL

Yes nice clean vsd jacquie!

Yes nice clean vsd jacquie! bidirectional. this is the most common congenital lesion in cats but looks compensated at the moment.

randyhermandvm

Can we discuss this

Can we discuss this bi-directional flow a bit more?

I assume the L to R flow occurs during ventricular systole- correct.

Is the R to L shunt occuring during ventricular diastole?

If the pressure is elevated in the R ventricle – would this not decrease the Jet into

the R ventricle during systole?

Is the right ventricle thickened here? Why isn’t there an indication of volume overload in the right side of the heart? I know the R atrium and Aorta are not usually in the flow for VCD

 

 

randyhermandvm

Can we discuss this

Can we discuss this bi-directional flow a bit more?

I assume the L to R flow occurs during ventricular systole- correct.

Is the R to L shunt occuring during ventricular diastole?

If the pressure is elevated in the R ventricle – would this not decrease the Jet into

the R ventricle during systole?

Is the right ventricle thickened here? Why isn’t there an indication of volume overload in the right side of the heart? I know the R atrium and Aorta are not usually in the flow for VCD

 

 

Pankatz

Good questions Randy! I think

Good questions Randy! I think the bi-directional flow is happening at the same time according to the waveform

I think the right heart can be very forgiving before you start to see changes -but with time it will be interesting to see what happens in this heart esp. if pulmonary hypertension sets in although I do think the IVS looks flattened which may indirectly indicate that this may be present but I am not sure.

I found it interesting that the pulmonary flow was higher than the arotic flow ( I usually find the opposite in normal hearts). In my simple mind to me this indicates more blood is going through the pulmonary artery (although still considered to be wnl)

We’ll see what the experts say

 

Pankatz

Good questions Randy! I think

Good questions Randy! I think the bi-directional flow is happening at the same time according to the waveform

I think the right heart can be very forgiving before you start to see changes -but with time it will be interesting to see what happens in this heart esp. if pulmonary hypertension sets in although I do think the IVS looks flattened which may indirectly indicate that this may be present but I am not sure.

I found it interesting that the pulmonary flow was higher than the arotic flow ( I usually find the opposite in normal hearts). In my simple mind to me this indicates more blood is going through the pulmonary artery (although still considered to be wnl)

We’ll see what the experts say

 

randyhermandvm

In a normal L to R shunt I

In a normal L to R shunt I would expect pulmonary pressure to be higher because of the increased volume. According to June Boon in Veterinary Echocardiography the normal shunt pathway for a VSD:

“Left vetricle => right ventricle=> pulmonary artery => lungs => left atrium=> left ventricle.

The right ventricle may not be dilated in hearts with VSD even though it is in the shunt pathway. Hearts with significant shunts usually have significant volume overloads.”

If anything I would believe you may be underestimating pulmonary flow unless this is truly a small shunt.

Normal pressures in Systole/Diastole:

L Ventricle:   120/10

R Ventricle:   20/5

If both the right and left side of the heart beat “nearly at the same time” explain how blood flows from a chamber with a systolic pressure of 20 (R Ventricle) into a chamber with a systolic pressure of 120 (L Ventricle). 

I could see right ventriculr pressure rising- forcing blood from the R Ventricle into the L ventricle during diastole.

I do agree that it appears you have bi-directional flow and your doppler seems to indicate this bi-directional flow above and below the base line, but I just have a hard time understanding this unless we are seeing a very stiff R ventricle – which means it should be thickened in comparison to the L ventricle (relative terms).

Do you have any M mode values?

I think your work is great- I just wish I could understand the changes here.

randyhermandvm

In a normal L to R shunt I

In a normal L to R shunt I would expect pulmonary pressure to be higher because of the increased volume. According to June Boon in Veterinary Echocardiography the normal shunt pathway for a VSD:

“Left vetricle => right ventricle=> pulmonary artery => lungs => left atrium=> left ventricle.

The right ventricle may not be dilated in hearts with VSD even though it is in the shunt pathway. Hearts with significant shunts usually have significant volume overloads.”

If anything I would believe you may be underestimating pulmonary flow unless this is truly a small shunt.

Normal pressures in Systole/Diastole:

L Ventricle:   120/10

R Ventricle:   20/5

If both the right and left side of the heart beat “nearly at the same time” explain how blood flows from a chamber with a systolic pressure of 20 (R Ventricle) into a chamber with a systolic pressure of 120 (L Ventricle). 

I could see right ventriculr pressure rising- forcing blood from the R Ventricle into the L ventricle during diastole.

I do agree that it appears you have bi-directional flow and your doppler seems to indicate this bi-directional flow above and below the base line, but I just have a hard time understanding this unless we are seeing a very stiff R ventricle – which means it should be thickened in comparison to the L ventricle (relative terms).

Do you have any M mode values?

I think your work is great- I just wish I could understand the changes here.

EL

Bidirectional flow starts

Bidirectional flow starts when eisenmengers physiology starts to kick in and the murmur grade starts to drop which is what you can monitor clinically and exercise intollerance starts as well if not sudden death. Nice discussion guys

EL

Bidirectional flow starts

Bidirectional flow starts when eisenmengers physiology starts to kick in and the murmur grade starts to drop which is what you can monitor clinically and exercise intollerance starts as well if not sudden death. Nice discussion guys

Pankatz

The m-mode values were wnl

The m-mode values were wnl for this patient and the LA size normal.

I find it hard to wrap my head around the physiology as well!

Pankatz

The m-mode values were wnl

The m-mode values were wnl for this patient and the LA size normal.

I find it hard to wrap my head around the physiology as well!

Peter

Hi!
1) you mentioned a

Hi!

1) you mentioned a continuous murmur – a VSD causes a systolic murmur only. Are u sure you didn’t miss a PDA here?

2) The right ventricle shows increased diameter and possibel increased wall thickness. This rules out congenital pressure overload. pulmonary hypertension is likely (or volume overload). This first is supported by the fact that the PCV was elevated (R-L shunt). PS or Double chambered right ventricle would cause pure concentric hypertrophy, no dilation

3) If there is pressure equalibration between the ventricles, the murmur gets very soft because there are not high velocities any more and the defect is usually large

4) If you want to line up a bidicretional shunt it is better to use PW to avoid any flow within the RV. Usually, flow into the right ventricle comes first, then the flow goes L-R. Never together!!! ( I think your CW is influenced by some other flow.

5) If you get a vmax of 5 m/s towards the transducer, then the pressure differences between the right and left ventricle are ok. This means, that the RV enlargement must be due to volume overload instead of pressure overload. Look for tricuspid dysplasia (most likely cause of RV volume overload)

6) If you check a VSD with color, always increase the nyquist limit to at least 1.2 m/s (or higher) to avoid too much aliasing. This makes interpretation much easier.

7) If it’s really a bididectional shut caused by a VSD and PHT, pulmonary artery banding might be an option although it’s not too likely for the PA pressures to decrease in a 13 month old cat (likely irreversible vascular changes…)

@Randy: Yes, very large defects always cause PHT due to increased flow. (Flow-mediated PHT). But this can lead to irreversible PHT due to vascular changes (media hypertrophy)

8) Don’t care about diastolic flow

9) Perform a bubble study to confirm R-L shunt

10) What makes me wonder is the continuous heart murmur in the face of a large right ventricle….. There must be a quite high systolic and diastolic pressure gradient within the great vessels. If there was much PHT then even a PDA would only cause a soft murmur…

Need all images of PA flow (up to bifurkation), AO flow, VSD with higher PRF setting, PW mappings across VSD (large sample volume), PA, AO.

Thanks for the nice case and discussion

Peter

Peter

Hi!
1) you mentioned a

Hi!

1) you mentioned a continuous murmur – a VSD causes a systolic murmur only. Are u sure you didn’t miss a PDA here?

2) The right ventricle shows increased diameter and possibel increased wall thickness. This rules out congenital pressure overload. pulmonary hypertension is likely (or volume overload). This first is supported by the fact that the PCV was elevated (R-L shunt). PS or Double chambered right ventricle would cause pure concentric hypertrophy, no dilation

3) If there is pressure equalibration between the ventricles, the murmur gets very soft because there are not high velocities any more and the defect is usually large

4) If you want to line up a bidicretional shunt it is better to use PW to avoid any flow within the RV. Usually, flow into the right ventricle comes first, then the flow goes L-R. Never together!!! ( I think your CW is influenced by some other flow.

5) If you get a vmax of 5 m/s towards the transducer, then the pressure differences between the right and left ventricle are ok. This means, that the RV enlargement must be due to volume overload instead of pressure overload. Look for tricuspid dysplasia (most likely cause of RV volume overload)

6) If you check a VSD with color, always increase the nyquist limit to at least 1.2 m/s (or higher) to avoid too much aliasing. This makes interpretation much easier.

7) If it’s really a bididectional shut caused by a VSD and PHT, pulmonary artery banding might be an option although it’s not too likely for the PA pressures to decrease in a 13 month old cat (likely irreversible vascular changes…)

@Randy: Yes, very large defects always cause PHT due to increased flow. (Flow-mediated PHT). But this can lead to irreversible PHT due to vascular changes (media hypertrophy)

8) Don’t care about diastolic flow

9) Perform a bubble study to confirm R-L shunt

10) What makes me wonder is the continuous heart murmur in the face of a large right ventricle….. There must be a quite high systolic and diastolic pressure gradient within the great vessels. If there was much PHT then even a PDA would only cause a soft murmur…

Need all images of PA flow (up to bifurkation), AO flow, VSD with higher PRF setting, PW mappings across VSD (large sample volume), PA, AO.

Thanks for the nice case and discussion

Peter

randyhermandvm

Thank you Peter, EL and

Thank you Peter, EL and Jaquiel. Good learning discussion.

randyhermandvm

Thank you Peter, EL and

Thank you Peter, EL and Jaquiel. Good learning discussion.

Pankatz

Thanks Peter –  great

Thanks Peter –  great information on scanning these cases! I am hoping to get a chance to re-scan this one in the future to get a better look.

Pankatz

Thanks Peter –  great

Thanks Peter –  great information on scanning these cases! I am hoping to get a chance to re-scan this one in the future to get a better look.

Peter

My pleasure 🙂

My pleasure 🙂

Peter

My pleasure 🙂

My pleasure 🙂

Skip to content