Liz Bode
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Replying to Caroline T. 24/12/2025 - 16:27
Hi Caroline,
This is a good question, what we mean by ‘normal’ velocity is the velocity we would expect to be generated by the right or left ventricle. Trivial MR or TR, in isolation (without valve changes) could be normal but if you are able to interrogate MR and TR and get a good profile then you probably have more than trivial regurgitation and that isn’t ‘normal’.
The RV is a low pressure system normally, so you would anticipate velocity of TR to reflect that, so a normal value for this is <3.0m/s. It is elevated in Pulmonic stenosis and pulmonary hypertension, amongst other more weird congenital abnormalities.
The LV is a high pressure system, so at normal blood pressure you would expect to see an MR velocity of 5-6m/s, reflecting a blood pressure of 100-120mmHg. MR velocity will be higher than this if there is aortic stenosis or systemic hypertension. It will be lower than this if there is increased left atrial pressure/ poor systolic function. However, in order to interpret the velocity of any jet accurately you must be critical of the profiles on Doppler you get, if you don't get a full profile then you can't interpret the image accordingly.
Hope that makes sense.
Liz
Replying to Annet Krabbenborg 14/12/2025 - 13:01
Hmmm, the noise around the baseline is possibly your wall filter? So you might want to increase that slightly to hide some of the noise.
Replying to Svetlana D. 12/12/2025 - 14:06
Hi Svetlana,
That looks good to me. You want to measure at the end of diastole, so the start of the QRS. Then leading edge to leading edge, so that is the top of the endocardium on the RV side of the septum and the top of the endocardium on the LV side of the septum and so on through the free wall, looks like your cursors are good here. Systole is the same but the smallest LV size, which is usually and of the T wave.
Liz
Replying to Svetlana D. 12/12/2025 - 14:06
Hi Svetlana,
That looks good to me. You want to measure at the end of diastole, so the start of the QRS. Then leading edge to leading edge, so that is the top of the endocardium on the RV side of the septum and the top of the endocardium on the LV side of the septum and so on through the free wall, looks like your cursors are good here. Systole is the same but the smallest LV size, which is usually and of the T wave.
Liz
Replying to Caroline T. 11/12/2025 - 08:22
Amazing! Welcome Caroline π
Answers to the above questions:
QUESTION 1 β Aortic Stenosis (Peak Gradient)
Doppler peak velocity across the aortic valve is 4.0 m/s. Calculate the peak pressure gradient between the left ventricle and the aorta.Solution
ΞP=4v^2= 4(4.0)^2= 4(16)= 64mmHgQUESTION 2 β Tricuspid Regurgitation (Estimating PA systolic pressure)
You measure TR jet velocity = 3.2 m/s. Right atrial pressure (estimated from CaVC) = 10 mmHg.
Calculate the pulmonary artery systolic pressure (PASP).
Solution
RVβRA gradient:
ΞP=4(3.2)^2=4(10.24)=40.96β 41 mmHgAdd RA pressure to estimate PASP:
PASP=41+10= 51 mmHgQUESTION 3 β Pulmonic Stenosis
The peak velocity across the pulmonary valve is 2.8 m/s. Find the peak systolic gradient.Solution
ΞP=4(2.8)^2=4(7.84)= 31.36 mmHgQUESTION 4 β Ventricular Septal Defect Gradient
You measure VSD jet velocity = 5.0 m/s. Calculate the pressure gradient between LV and RV.Solution
ΞP=4(5.0)^2=4(25)= 100 mmHgQUESTION 5 β A step further: Estimating RV Systolic pressure from VSD velocity
If systemic systolic BP = 100 mmHg and VSD jet velocity = 4.0 m/s, what is the RV systolic pressure?Solution
Gradient:
ΞP=4(4.0)^2= 64 mmHg
RVSP=SBP-ΞP=100-64= 36 mmHgReplying to Annet Krabbenborg 03/12/2025 - 19:45
Hi Annet,
Thanks for the questions, tissue Doppler is a little tricky! In terms of the annulus, yes this is where the valve attaches to the wall of the heart, it is also called the hinge point.
When setting up tissue Doppler, I narrow the sector width, then put the colour on to cover the whole window (you might also need to adjust the depth to get the frames per second above 200), you will also need to adjust the Nyquist limit so you don’t get any brown colour. Then I place the sample volume of the pulse wave Doppler (which is how I set it up on my machine, but it could be different on other machines) on the annulus. The sample volume is usually 2-3mm.
Hope that helps!
Liz
Hi Riley,
Thanks for posting this, it is a super interesting and exciting development in both people and animals. In people, they found that these drugs were of significant benefit to those with DM in terms of CV outcomes. They have then also found a significant benefit to people without DM but with CHF caused by both systolic and diastolic dysfunction. They survive for longer and have less hospitalised patients. There is a strong interest in veterinary medicine, not least because there is already a licensed product in cats. I am sure drug studies are already underway (in fact I know they are) so we are just waiting for the data…
Watch this space…
Liz
Replying to Emma Holt 24/11/2025 - 12:00
Hi Emma,
Frustrating isn’t it!!! Do you use the Vivid? We have the same problem. We find that attaching the ECG to the feet prevent this to some degree, we use crocodile clips (flattened ones) for environmental reasons mainly and the baseline does tend to wander quite a bit. Sometimes, if we attach them to the feet it does this less. Another problem is if one of the lead touches another, which happens commonly in cats. If you can keep them separated it tends to move about less. Otherwise, we just have to put up with it π
Liz
Replying to Emma Holt 24/11/2025 - 12:00
Hi Emma,
Frustrating isn’t it!!! Do you use the Vivid? We have the same problem. We find that attaching the ECG to the feet prevent this to some degree, we use crocodile clips (flattened ones) for environmental reasons mainly and the baseline does tend to wander quite a bit. Sometimes, if we attach them to the feet it does this less. Another problem is if one of the lead touches another, which happens commonly in cats. If you can keep them separated it tends to move about less. Otherwise, we just have to put up with it π
Liz
Replying to Roland R. 17/11/2025 - 10:36
Lovely to have you join us π
I also love South Africa π
Replying to Graeme E. 10/11/2025 - 10:03
Hi both,
Interesting paper! I think (anecdotally) they probably do worse, but I can also think of many that don’t. We were chatting about this yesterday and we discussed giving cats any prognosis is difficult, because some with awful looking hearts can do very well and vice versa, whereas dogs are more predictable.Yes, Rachel did present that at VCS. I would caveat that though to say it was a very small cohort and we have no further evidence. There are potential issues with giving animals with left-sided heart disease sildenafil and those are related to the fact that if you dilate vessels in the lungs and make it easier for blood to flow from the right to the left that you can then worsen left-sided heart failure as you flood the LA with more blood, increasing it’s pressure. So, until we have further, better quality evidence, I would hold off sildenafil for now π
Hope that is useful,
Liz
Hi Lucy
Thanks for the good question. This is purely down to heparin’s bioavailability via the s/c route vs i/v. The risk of haemorrhage is significantly higher via the i/v route so should be avoided in these patients. Low Molecular weight heparin is preferred as it is more predictable in nature.
Hope that is helpful.
Liz
No takers on this one (I’m hoping the loops were working for you as now they are shoing an error). The loops are pretty short as we have to save them like this to reduce the space they take up!
The FAST scan β shows a low volume pleural effusion. In the other view, the walls look hypertrophied, septum and free wall, the LA looks dilated and systolic function look normal.
So, we now have to assume that this cat has a pleural effusion secondary to L-sided CHF and an HCM phenotype. This then leads on to treatment and further tests, as follows:
No thoracocentesis as low volume pleural effusion
We checked haem and biochem (inc electrolytes) and all was within normal limits.
Blood pressure 136mmHg
Cardiac troponin I = 1.5ng/ml (ref <0.04)
ECG - sinus tachycardiaSo we gave the cat 2mg/kg IV furosemide and started clopidogrel.
Based on the troponin I results we had the differentials of myocarditis and ischaemia. We followed this up with Bartonella PCR, FIV/FeLV and Toxo serology. The cat was positive for Bartonella. Of course, this could be a coincidence, cats can 'carry' Bartonella, but given the troponin etc we decided to treat. Sadly the cat was lost to follow-up,
Replying to Christina Frigast 01/08/2025 - 13:22
Hi Christina,
No problem. I love arrhythmia and CHF management π one of my favourite areas of cardiology.
I think lack of rate control could be partly associated with poor appetite/ general malaise. You reduce your cardiac output by 20-25% in AF (no coordinated atrial contraction) and then if you add on to this the lack of rate control then cardiac output will drop again. To add insult to injury, if you have poor right sided systolic function then you will move less blood to the left side and further reduce left sided cardiac output which can also make them feel poorly. So, there are many reasons.
If her average HR over 24 hours was >125bpm on diltiazem then I would either increase the dose and evaluate response, or add in digoxin. The latter is likely to be more successful but could worsen reduced appetite etc. You also sometimes see ventricular arrhythmias on Holter and in those cases sotalol might be better. It is often a fine balance and can be trial and error to find the ‘right’ combination.
Liz
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