V TACH in collapsed labrador

Re: V TACH in collapsed labrador

Ruth Willis — Fri, 21 Jan 2011 21:04:01 GMT

Hi Alex,

My experience of St B SVT is that they don't respond well to beta blockers or diltiazem but do respond well to sotalol.

However it think in these cases Holtering before and after therapy is essential to show that you have made a significant difference (for better or worse) before changing therapy.

Dog's can die from SVT as well as VT due to compromised myocardial perfusion at high HR so the presence of R-on-T / couplets (which are common in dogs with significant SVTs) may not have been the trigger of the terminal rhythm but who knows... All supposition and a taste of life in the [almost] evidence free world of canine anti-arrhythmic therapy.

Ruth Willis BVM&S DVC MRCVS, Holter Monitoring Service

Re: V TACH in collapsed labrador

Alex Gough — Fri, 21 Jan 2011 13:54:15 GMT

Hi Ruth, interesting comments re R on T. I do use it as a warning flag to consider anti-dysrhythmic treatment. I had a weird case recently, juvenile St Bernard with idiopathic supraventricular tachycardia (heart rate 300bpm) which didnt respond to lignocaine, but converted to sinus rhythm with a precordial thump, and was followed up with diltiazem. It was doing well, but when I saw it back after 2 months of doing well and re-ECGd, I saw a normal sinus rhythm, with intermittent VPCs, and one close-coupled pair of VPCs/R on T in a 5 minute strip. I was waiting 24 hours for the diltiazem to wash out prior to starting sotalol, and the dog dropped dead at home that afternoon.

Alex

Re: V TACH in collapsed labrador

Andrew Mellor — Fri, 21 Jan 2011 10:09:04 GMT

Ruth you are so right , post surgery he had a sotolol and we thought we were going to loose him,rate dropped and he colapsed again fluids etc stabilised him but 24 hours later when sotolol gone up bouncing around, I am learning so much from you all. could anyone tell me exactly what lidocaine they use for these cases

Re: V TACH in collapsed labrador

Ruth Willis — Thu, 20 Jan 2011 21:31:30 GMT

Hello,

Chipping in a bit late here... I could be controversial and say that cardiologists have busier days than medics but that would probably be unwise. :-)

Thanks Mike for great summary re accelerated idioventricular rhythms.

I have been looking at the trace and assuming paper speed is 25mm/s (as written on it) and [unless I'm missing something!] therefore the time between two of the large dark squares at the top of the trace = 3s making the rate is consistently greater than 180bpm so I would classify what we're looking at here as polymorphic ventricular tachycardia. Polymorphic VT in human literature is defined as continuously changing or multiform QRS morphology (ie no constant morphology for >5complexes, no clear isoelectric baseline, and/or QRS complexes which have different morphologies in different leads indicating variable sequence of ventricular activation and no single site of origin). In dogs I tend to use cut off of >180bpm for VT.

Whilst this might sound like an issue of semantics I think this is clinically relevant as the faster the rate, the more likely that cardiac output will be adversely affected which brings us back to Mike's point that blood pressure and clinical findings are relevant.

The issue of when to treat ventricular arrhythmias is a minefield... On Holters you can see horrific looking VT whilst the patient diary suggests that the dog is oblivious. I'm also not convinced that R-on-T matters in dogs (and how do you define it anyway) but that's prob a topic for another day. However in the context of polymorphic VT secondary to systemic disease with a hypotensive sympatomatic patient I think lignocaine is likely to be the drug most like to be effective and least likely to harm. The rationale for this is that lignocaine (and same applies to mexilitene) tends to affect myocardial tissue preferentially to pacemaker tissue - ie it acts on the ectopic focus and works by slowing the upstroke of the action potential thereby reducing the likelihood of a bit of non-pacemaker tissue reaching it's threshold potential and therefore the ectopic focus is suppressed. Lignocaine on the whole is well tolerated and, in my opinion, carries a low risk of pro-arrhythmia.

Conversely sotalol tends to prolong phase 3 of the action potential in both pacemaker tissue and cardiomyocytes - as MIke pointed out, slowing the sinus rate could actually enhance an AIVR and, as sotalol is less effective at higher heart rates (reverse use dependence), it becomes less efficacious as HR increases. In the situation of the myocardium adversely affected by systemic disease (so hypoxic, acid-base disturbance, electrolyte disturbance, etc, etc) I think it is likely that you would get a variable effect on the AP duration of cardiomyocytes with sotalol and therefore could create a more electrophysiologically heterogenous myocardium thereby creating possible conditions for pro-arrhythmia. Additionally sotalol is a negative inotrope so cardiac output could be further reduced. I think sotalol is a great drug and has a place in the anti-arrhythmic armoury but maybe not this setting but I'm happy to be corrected.

Fascinating discussion!

I hope the dog does well.

Ruth Willis BVM&S DVC MRCVS, Holter Monitoring Service

Re: V TACH in collapsed labrador

Alex Gough — Thu, 20 Jan 2011 16:19:34 GMT

Been thinking a bit more about this, Mike. I'm sure I was taught or read during my cardiology cert that slow vt was the old terminology for accelerated ventricular rhythm, and it was abandoned as terminology because it isn't actually tachycardia if it is less than 160-180 bpm. I see from your explanation and more googling that the situation is more complex than that. How important do you think it is to differentiate clinically between a slow VT and AIVR?

alex

Re: V TACH in collapsed labrador

Andrew Mellor — Wed, 19 Jan 2011 19:09:24 GMT

Thank you so much for all the time you have taken over this Mike, the tracing was so all over the place with so many different wave forms and so much variability I was thinking oh this has to be bad but in actual fact that irregularity is a good sign ( from a heart point of view) just need to find and treat the underlying cause.

The old boy is doing really well now the heart has already started to stabilise and he is up and about, looking to discharge tomorrow.

Re: V TACH in collapsed labrador

Alex Gough — Wed, 19 Jan 2011 18:14:37 GMT

Thanks Mike, really clear and interesting explanation of the phenomenon.

Alex

Re: V TACH in collapsed labrador

Mike Martin — Wed, 19 Jan 2011 16:41:59 GMT

An example of the long coupling interval, and often variable coupling interval too. The black lines show the distance from the 'normal' beat to the ventricular ectopic.

Re: V TACH in collapsed labrador

Mike Martin — Wed, 19 Jan 2011 16:40:41 GMT

An example of the slightly irregular rhythm. The arrows point to the variable length of baseline between beats. This is the single most useful feature. Then there is a lovely fusion beat at the end of this run.

Re: V TACH in collapsed labrador

Mike Martin — Wed, 19 Jan 2011 16:39:10 GMT

An example of fusion beats - the mix of a normal beat and a ventricular ectopic. This creates bizzare and variable shapes.

Re: V TACH in collapsed labrador

Mike Martin — Wed, 19 Jan 2011 16:37:18 GMT

With the help of Google, I've attempted to draft a description of this. There is nothing in vet books I can find that is particularly useful. And then I'll post some examples......

Accelerated idioventricular rhythm (AIVR) is defined as an enhanced ectopic ventricular rhythm, which is faster than normal intrinsic ventricular escape rhythm, but slower than ventricular tachycardia.

AIVR is generally a transient rhythm, rarely causing haemodynamic instability and rarely requiring treatment. However, misdiagnosis of AIVR as slow ventricular tachycardia or complete heart block can lead to inappropriate therapies with potential complications. AIVR is often a clue to certain underlying conditions - in particular various abdominal or medical conditions in dogs such as gastric dilation, pancreatitis, splenic masses, electrolyte imbalance, etc...The mechanism of AIVR appears to be related to the enhanced automaticity in His-Purkinje fibres and/or myocardium, sometimes accompanied with vagal excess and decreased sympathetic activity.When the enhanced automaticity in His-Purkinje fibre or myocardium surpasses that of sinus node, AIVR manifests as the dominant rhythm of the heart. Sinus bradycardia may facilitate the appearance of AIVR.

Usually, AIVR is haemodynamically well tolerated due to its slow ventricular rate. It is self-limited and resolves as sinus rate surpasses the rate of AIVR. Rarely, AIVR can degenerate into ventricular tachycardia or ventricular fibrillation.

The following are ECG features of AIVR:

The rate is typically between 100-180/min (sometimes up to 200/min)
It is not metronomically regular, with some variation being present, and gives the impression of spacing between beats of variable length.
The morphology of complexes is often variable, in part because of fusion complexes, but also there seem to be runs of one morphology and then a run of a different morphology.
AIVR starts gradually as a long-coupled, premature ventricular beat.
At the onset of AIVR, the rates of AIVR and sinus rhythm are often similar; therefore, it is common to see ventricular fusion beats.
Often a gradual onset and termination of AIVR are helpful in differentiating it from slow VT, which is associated with sudden onset and termination.

The most important therapy for patients with AIVR is to treat the underlying aetiology.

AIVR is usually haemodynamically tolerated and self-limited; thus, it rarely requires treatment.
In some situations, atropine can be used to increase the underlying sinus rate to inhibit AIVR.

Re: V TACH in collapsed labrador

Andrew Mellor — Tue, 18 Jan 2011 11:42:50 GMT

hows that ?

Re: V TACH in collapsed labrador

Mike Martin — Tue, 18 Jan 2011 11:00:24 GMT

Well done for finding the haemoabdomen!

The only other thing to add....

With any scary arrhythmia - check the blood pressure. If low (<100 mmHg systolic) then it is causing haemodynamic compromise (ie shock-like) and if >110mmHg - there's usually less concern/rush/panic.

An idioventricular rhythm is commonly seen with non-cardiac diseases (looks like a slow VT). Rate is one loose guideline as Alex said, but the ECG also looks different from cardiogenic VT. Can you scan in a copy of the ECG and post it here and I could try to explain. There is a lot of debate on whether antiarrhythmic drugs should be used on these - I tend NOT to.

With fluids, nursing and time, the idioventricular rhythm should resolve without specific drug treatment.

Re: V TACH in collapsed labrador

Andrew Mellor — Tue, 18 Jan 2011 10:34:48 GMT

have avoided the exploded part which just looks like haematoma and sent a slice from the edge of the lesion including what looks like normal tissue so the boundaries can be seen, had not thought of the bread slicing trick though I will do that next time , thanks Richard.

Has anyone got an idea how long the vtach will last for now the spleen has been removed, ecg looks more normal ie there are some normal complexes as well as escape beats but still the majority are ectopics. dog definately brighter though and crt now 2 seconds and there is some colour in his gums, started him on Sotalol yesterday prior to surgery.

Re: V TACH in collapsed labrador

Richard Fox — Mon, 17 Jan 2011 21:22:24 GMT

Can I advise you either slice it up like bread but keeping the spleen together like a book (don't cut all the way through - to aid fixation) or keep it in a bucket after slicing and send representative bits off - esp not the bloody bits (generally blood!) the bits best are paler parts and altered tissue under the capsule :)

I have seen loads of different type of lesions cause splenic rupture apart from trauma & HSA etc inc myelolipomas, nodular hyperplasia, fibrohistiocytic nodules, lymphoma........

Re: V TACH in collapsed labrador

Mark Hedberg — Mon, 17 Jan 2011 20:21:11 GMT

[quote user="Andrew Mellor"]

they just don't know when to quit !

[/quote]

And lucky for us, too!

Re: V TACH in collapsed labrador

Kate Richardson — Mon, 17 Jan 2011 18:13:06 GMT

Well done, hope he keeps getting better

Re: V TACH in collapsed labrador

Andrew Mellor — Mon, 17 Jan 2011 17:59:06 GMT

ruptured spleen but does not look tumourous just old dog spleen, obviously will send off for histo. dog looks so much better colour already heart still not terribly strong, amazed he survived the surgery, still after all my experience as a vet animals still amaze me ! they just don't know when to quit !

Re: V TACH in collapsed labrador

Alex Gough — Mon, 17 Jan 2011 17:28:02 GMT

Splenic tumours are a common cause of ventricular arrythmias. What did you find?

alex

Re: V TACH in collapsed labrador

Kate Richardson — Mon, 17 Jan 2011 15:58:22 GMT

Nothing on abdo scan otherwise? Let us know what you find!

Re: V TACH in collapsed labrador

Andrew Mellor — Mon, 17 Jan 2011 14:09:53 GMT

echo normal but did find some free fluid in abdomen, numerous attempts at paracentesis and eventually with 3 inch needle got through the fat and blood free in abdomen - it didn't clot so looking to open up in a couple of hours and wade through the fat !

thanks for all your advice

Re: V TACH in collapsed labrador

Kate Richardson — Mon, 17 Jan 2011 13:37:42 GMT

If the tachycardia is caused by pericardial effusion/haemorrhage, then pericardiocentesis should go a long way to resolving the tachycardia? and make the dog much much more stable, literally see them improve in front of your eyes, quite amazing. Agree, very scary the first time you do it, but not that difficult and you're in a position where you have nothing to lose really because the dog is going to die if you don't. Amazing feeling when it works! Real ER moment!!!

Re: V TACH in collapsed labrador

Richard Fox — Mon, 17 Jan 2011 11:50:13 GMT

I'm also thinking of a RA HSA - as these can present with acute pericardial H+ and thus similar to a pericardial effucsion can lead to VTAC IIRC - However I guess you would need to try and get the HR down if it is causing clinical signs i.e. dog is unstable, first?

Re: V TACH in collapsed labrador

Martin Jones — Mon, 17 Jan 2011 11:34:05 GMT

Another firm vote to have a look for pericardial effusion. Can certainly be due to heart base tumour, so looking for other lumps is useful, but I have a feeling that I was taught that fat labs are a bit prone to idiopathic effusions? Diagnosis is relatively straightforward, even for a dullard like me. Blind / US-guided drainage is an option to immediately relieve some of the tamponade, and is half as difficult and twice as scary as it first appears.

Any potassium levels done?

Re: V TACH in collapsed labrador

Kate Richardson — Mon, 17 Jan 2011 11:20:48 GMT

Def stick ultrasound onto heart- pericardial effusion easy to pick up- have had a couple of pericardial haemorrhages here recently,1 secondary to met from splenic tumour (assumpitive diagnosis as not histo done), the other idiopathic pericardial haemorrhage.