Liz Bode
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Hi Marina,
These are good questions. We aren’t really sure what causes the CHF in cats with steroids – it could be that going to the vets and experiencing a stressful event, such as steroid injection or diagnostic tests that then result in steroids are enough to result in CHF via TMT. However, steroids cause fluid shifts in cats and if there is any diastolic dysfunction, be that HCM or ageing, then the heart will be less able to cope with these fluid shifts and the LAP can increase causing CHF. Steroids in this situation wouldn’t cause TMT but CHF in a more direct manner. TMT is thought to be stress induced/ myocarditis like in nature.
Difficult to know in your cats, especially if they have had a normal echo prior to steroids, what the cause was. Stress could be an inciting factor, immunosuppression could have made the second cat more prone to viral infection and myocarditis, steroids themselves, or other infiltrative processes like lymphoma can also cause CHF.
In general, we will echo cats prior to steroids, but we don’t usually see many issues if their hearts are normal prior to administration. That being said, it is always a good idea to wean down/ stop steroids as soon as feasibly possible where you can.
Sorry, no clear answer but food for thought!
Liz
Hi Zenobie
In regards to your image, you have drawn the chin and beard correctly with respect to more accurate velocity and, therefore, pressure gradients.
The transit time effect contributes to the ‘beard’ appearance on spectral Doppler by causing spectral broadening. As red blood cells pass through the sample volume, they are detected for a finite period of time, resulting in a spread of Doppler frequencies rather than a single frequency. This creates an apparent range of velocities on the spectral Doppler display, even when the actual blood flow velocities are similar. As there is a range of velocities they are not cancelled out.
Hope that makes sense.
Liz
Hi Scott,
I think this is in interesting drug, and in people has become part of the standard of care for heart failure. I have a couple of problems with this paper (I am surprised it was published in JVIM);
– the main one is the way they report survival time. They represent survival time predominantly from the diagnosis of CHF, not the start of Entresto, therefore we have no evidence that it prolongs survival time. There is a little survival data from the start of Entresto later on in the paper, but there is no control group so we can’t draw any firm conclusions
– it is a relatively small sample size when you drill down in to it, so it is more of a case series.The drug in the UK (even from a human pharmacy) is VERY expensive, we costed it for one of our clients with a chihuahua and it was going to be £300/ month at the starting dose. You have to be wary of renal function and monitor that and BP closely, adding cost to the client.
All that being said I would consider it in my hard to control stage C dogs or stage D!
Liz
Replying to Zenobie H. 18/09/2026 - 00:44
Hi Zenobia,
Unfortunately, this really depends on the machine that you have and the probes. If the machine is relatively new you should be able to get the company back in to your practice to adjust the pre-sets to your requirements/ personal preferences. The latter also forms some of the pre-set as some people prefer an image that is highly gained for example.
Sorry that I am not much use with this one.
Liz
Hi Fiona,
For dogs we use trazodone +/- gabapentin the night before and morning of the appointment, if we know that they are going to be anxious. However, more often than not we don’t and so they then tend to get either butorphanol IV or IM. If we have to do that then we go for doses of 0.3-0.4mg/kg, ideally IV. I will also add this to the gaba/ trazodone at the same dose if needed, prior to reaching for anything like alfaxalone. However, I’d say for the majority of dogs either gaba +/- trazodone OR butorphanol is adequate.
For cats we would give them 100mg gabapentin the night before and the day of the appointment. Then if required we would use a top up of butorphanol IV ideally, at the same doses as for the dogs. However, invariably if we have to do this then we end up using alfaxalone IV too. Rarely would we have to reach for anything more.
We always scan lying down, unless it is a POCUS. We are lucky that we have a dedicated cardiology room, which is dark and very quiet so the majority of cats we manage just fine with 2 handlers without anything more. Gaba works very well though if needed. Only those very nervous/ aggressive cats need more than this.
Hope that is helpful!
Liz
Replying to Fiona C. 27/08/2026 - 15:40
Hi Fiona,
It is a good question, but generally, even if tamponade is present, we don’t drain these. The ones that I have seen the tamponade is mild. I have seen cases that have been drained and end up with huge blood clots in their pericardial space. Obviously if the dog is in cardiogenic shock that might be different, but in that case I would give them a fluid bolus and try to improve cardiac output that way and see how they respond to that before draining them. That being said, I have also a drained pericardial effusion which I later suspected to be due to a LA tear, and the dog was fine and didn’t develop blood clots!
There’s no hard and fast rule, but generally the advice is to leave them alone, and hospitalise them for monitoring.
Liz
Replying to Emma Riley 25/06/2026 - 21:09
Hi Emma,
As a screening tool for HCM/ severe heart disease in cats it could be helpful, but I don’t think I would use it in all older cats pre-GA. I think it might be sensible to include it if you had a murmur/ arrhythmia/ gallop sound or any of the other risk factors we discussed. However, it will miss a significant proportion of cats with mild/ moderate disease and might lull you/ owners into a fale sense of security if it was used routinely.
In terms of troponin, I do measure it in all cats with HCM-phenotype on echo (if clinical for it at least), the main reason being that myocarditis is a differential for an HCM phenotype. We don’t tend to use it in pre-clinical, unless there was an arrhythmia we were investigating, for example. Mainly because myocarditis could also manifest itself that way.
Best wishes,
LizReplying to Emma Riley 23/06/2026 - 13:04
Great! I am sure if you choose Beecardia you will like it 🙂
Replying to Emma Riley 16/06/2026 - 15:44
Hi Emma,
No, no need to have paper ones we use digital in our practice (although I still prefer paper traces lol!).
Many people reeally like the Beecardia system, it works off a tablet, is very portable and circa £1500-2k so not terrible price wise. It is a cloud based system and takes a good trace. My gripe with it is that it was slow to start up and then you couldn’t review live ECG traces, you have to save them and log on to the cloud. We have the dextronix system, and whilst this allows review in real-time, it also has frustrations. It is a similar price point. If I had to choose I would probably go back to the Beecardia!!
Let me know what you choose!
Liz
Replying to Liz Bode 07/06/2026 - 19:53
Hi Emma,
Sid answered:
We didn’t do any further investigations, started amox-clav and doxy (alongside furosemide and clopidogrel), the cat passed away at home a week later.
Endocarditis cases go one way or the other in my experience, they either survive beyond expectations or die suddenly in a relatively short time frame 🙁
Liz
Replying to Emma Riley 02/06/2026 - 11:38
Hi Emma,
I will reach out to Sid and get back to you once he has responded.
Liz
Sorry this took so long to reply too, I was waiting for info from Oscar as it was beyond my expertise 🙂
Hi Julia,
Great question – it’s a really interesting point and one that’s a bit controversial taking into account how we’re usually taught to be cautious with alpha-2s in cardiac patients.
What I meant is that the effects of dexmedetomidine (and medetomidine as well) are very dose-dependent. At “normal” doses or when given as a bolus, you get the classic picture – peripheral vasoconstriction, reflex bradycardia, and a marked reduction in cardiac output. That is obviously not ideal in many cardiac cases.
However, if you use very low doses as a CRI, you could avoid that plasma peak increase and mainly get the central effects (sympatholysis) without much peripheral vasoconstriction. In practice, that means less catecholamine release, less tachycardia (and bradycardia), reduced myocardial oxygen demand, and generally smoother haemodynamics. That’s where the idea of “cardioprotection” comes from.
In terms of when to use it, I usually think about relatively stable cardiac patients (for example compensated MMVD) where tachycardia or stress responses could be contradictory. It’s not something I would use for in unstable patients. I’d usually start the CRI after induction, once things are stable, and use it as part of maintenance to help with surgical stimulation and reduce inhalant requirements.
For dosing, a typical dexmedetomidine CRI would be around 0.25–1 µg/kg/hour, starting at the lower end and titrating to effect. The aim is trying to remove its sympathetic tone if that makes sense. If dexmedetomidine is not available, medetomidine can be used doubling the dose.
So overall, it’s less about using alpha-2s as “sedatives” and more about using them as a very fine-tuned way of controlling sympathetic tone.
Hope that helps a bit – it’s definitely one of those areas where small dose titration make a big difference!
Thank you
Oscar
Replying to Julia Biernat 11/04/2026 - 09:14
Hi Julia,
No problem!
1. Can we tell from these that the Vtach is right sided? The complexes are positive in lead II which would suggest that these complexes come from the right ventricle.
2: I calculated the HR at 180 is that correct? counted 10 large squares as 1s. I don’t tend to count the squares on an ECG like this, my eyes always make me get different answers from a screen (I am old fashioned an need a printed copy). If you look along the very top of the ECG you will see some markers and numbers after them. These markers correspond to the QRS complexes and are in milliseconds. You can work out an instantaneous rate by dividing 60,000 by the number e.g. 60,000/ 230 = 260bpm.
3: Can we tell from these that it’s Mobitz type II and that’s more advanced disfunction than type I or does it not really matter? This looks like Mobitz Type I – the PQ interval appears to prolong slightly before the blocked P wave and then the PQ after the blocked P wave is shorter again, characteristic of Mobitz type I which tends to be more physiological. Type II tends to be more pathological (although not always pacemaker territory).Hope that helps.
Liz
Replying to scott@vtx-cpd.com 30/03/2026 - 00:31
Our anaesthetists would use dexmedetomidine (or other alpha-2) in cats with HCM, the main reason being is that HCM is a disease of diastolic function and systolic function is often preserved (unless end-stage), so the alpha-2s will have limited adverse effects on cats. They usually use a low dose (I am sure Oscar discussed this in his webinar), together with an opioid. Cats also less commonly have mitral regurgitation, which would be another contra-indication to using this class of drug (they increase afterload and so can worsen regurgitant fraction through the mitral valve).
Thanks for sharing! Yes, this is what we already know, that systolic function cannot be interpreted. Its use in cats is less worriesome as they have diastolic disease (although they can get issues with systolic function too).
Liz -
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