Looks like some bronchial
Looks like some bronchial disease and chest fat, The la max is not scary but if june boon method of 1.6 in correct position would be enlarged, Rishniw high normal. How about inspiratory/expiratory tracheal rads? The pulmonary artery and vein appear pretty normal so don’t think overt left chf but main stem bronchus impingement by LAE may be playing a part but likely more respiratory and maybe the heart looking in. Any chance of uploading the heart base and 4 chamber long axis echo views? Allergy season starting too. Funny how when my allergies start the respiratory coughs start up and the cardiac vs respiratory discussion starts kicking in:)

My thought is bronchial
My thought is bronchial airway disease as well but I would have hoped better response to pred.

I have talked to owners about repeating rads as well as these were not taken at my hospital. Also getting x-ray of the laryngeal region and perhaps upper GI barium as pet was doing some regurgitating prior to the cough but not any longer.

I will try to post some of the echo when I get a chance.

Thanks!

Hi!
Wondering why there´s no
Hi!
Wondering why there´s no concentric hypertrophy present in the presence of SAS (any significant aortic regurgitation?)
Based on the rads I would consider a respiratory problem responsible for cough. Bronchial (broncho-interstitial) pattern and concomitant cardiomegaly with LAE.
a 4 and 5-chamber view (video) would be perfect. A bronchoscopy would be indicated. Otherwise you could as well try theophylline at 5-10 mg/kg bid.
Peter

Hi Peter
Thanks for chiming
Hi Peter
Thanks for chiming in. I did not see aortic regurgitation. According to my reference tables (provided by June Boon) there was mild increase in LV wall thickness for a 13.2 kg dog
IVSd 10.5 (7.9-9.0)
PWd (7.6) (6.3-7.2)
But LVDd was also increased 39.7 (24.1-35.8)

I understand that SAS is an afterload disease so we should see concentric hypertrophy. I was thinking that perhaps concurrent MVD was contributing to the change in LVDd (preload disease) and that the SAS was not severe enough esp. since this pet had lived this long with it. Of course operator error (in myself) can not be ruled out!

But I am glad that you agree that at this stage, the cough seems to be of respiratory origin.

I will try to get some of the echo posted in the near future.
Jacquie

I have posted some clips and
I have posted some clips and stills in the above original post.

Now looking closer, I do think there is mild aortic regurgitation in which I also posted a still of. It looks like it is at the start of diastole. And in doing some reading, it looks like a large percentage of AS cases should have regurgitation. What do you think?

The LVOT does not look too abnormal to me- maybe a little “bleb” just before the aortic valve? – is it possible to have SAS without any standout lesions?

The MR in the clip above does not look as severe as I saw in other views but does show it.

Thanks for your help and advice!
Jacquie

Yes there looks like some AI
Yes there looks like some AI and its easy to miss on spectral Doppler as at times the jet is very thin like TR in PHT cases that have good TV structure and apposition…. easy to miss.

Back to the LA size and the cough the LA is slightly enlarged subjectively in the heart based view but I don’t think enough for main stem bronchus cough but the enlargement is mostly right sided which you will see in a lot of respiratory cases especially on rads if you snap the rad during diastole.

Usually in sas cases there is Ai and often MR like this guy. Just a matter of lining up and dropping the cursor in the exact spot. Most MR jets shoot toward the la free wall but occasionally toward the AS so trying in both regions or right at the valve apposition usually minimizes the possibility of error.

i totally agree: The LVOt is
i totally agree: The LVOt is narrowed and there´s some evidence of poststenotic dilation. Additionally, the MI is also diastolic ! There are no p-waves on the ECG -> atrial standstill??? Pls. perform an ECG recording in this dog! If also evident on the ECG, I would perform an atropine-response test (0.04 mg/kg Atropine i.m, record ECG every 5 min, HR should exceed 140/min within 20 min, Pwaves should be visible again – > but it´s unlikely….).
Atrial standstill is frequently seen in Spaniels. The diastolic regurgitation if the MV is functional. A pacemaker is often indicated. Diastolic dysfunction is also a consequence -> increases LA size additionally. Furthermore, due to the low heart rate, the LVOT peak velocity can increase functionally because of the increased diastolic filling.
I would start with a combination of ACEI and Spironolactone to decreased preload.
I woudl also be happy if you could keep me updated on this case…
(and I would re-auscultate the patient because you might hear a diastolic murmur 🙂 )

Peter

Diastolic MR? That is a new
Diastolic MR? That is a new one for me! I will get a hold of the owners to see if we can get an ECG on this pet. I can run it on my Cardell (which I think is only a lead three) or would it be better to just do a Cardiopet consult?

Could these things be causing the cough in this patient or is this a separate problem?

Will definitely keep you updated
Thanks
Jacquie

Looking at the case and the
Looking at the case and the posts, there is no doubt cardiac disease and possibly contributing to the cough but tend to agree with Peter that respiratory disease needs to be ruled out by means of bronchoscopy and TTA. There is more evidence of respiratory induced cough than cardiac induced cough – no exercise intolerance, no nocturnal cough, SRR of 30-35, tracheal sensitivity, and some response to steroids.

A recent study highlights these findings – Study to be published in Journal Vet Internal Medicine:

Risk Factors for Coughing in Dogs with Naturally Acquired Myxomatous Mitral Valve Disease
L. Ferasin, L. Crews, D.S. Biller, K.E. Lamb, and M. Borgarelli

Background: Cough often is reported as the primary clinical sign of congestive heart failure (CHF) in dogs with chronic degenerative myxomatous mitral valve disease (MMVD). Concurrent airway disease and compression of the left mainstem bronchus by a large left atrium also have been proposed as potential causes of coughing in these patients.
Objectives: To investigate the association between the presence of coughing and different potential causes of cough, including CHF, abnormal radiographic airway pattern, and cardiomegaly in dogs affected by naturally acquired MMVD.
Animals: Two hundred six client-owned dogs.
Methods: Retrospective analysis performed on medical records of dogs affected by MMVD that underwent full cardiac evaluation, including echocardiographic examination and thoracic radiography.
Results: Univariate analyses showed that CHF is not a predictor of coughing (OR = 1.369; 0.723, 2.594), whereas abnormal radiographic airway pattern (OR = 3.650; 2.051, 6.496) and increased left atrial size observed radiographically (OR = 3.637; 1.904, 6.950) or echocardiographically (OR = 2.553; 1.436, 4.539) were significantly associated with coughing in dogs with MMVD. The same risk factors were significant in multivariate analyses.
Conclusions and Clinical Importance: This study indicates that CHF is not significantly associated with coughing in dogs with MMVD. Instead, abnormal radiographic airway pattern and left atrial enlargement are associated with coughing in these patients. This important finding should be taken into account when considering diagnosis and clinical management of CHF in these dogs.

I totally agree with you,
I totally agree with you, Remo and I think this matches the experience of most cardiologists/internists. Still, no one knows, if medical treatment aiming at reducing LA pressures will effectively reduce the mechanical irritation of the left mainstem bronchus and therefore improve the respiratory issues because some dogs with airway disease and without cardiac disease respond to Furosemide, probably because of the suspected antitussive effect of loop diuretics.
Re the atrial standstill. if vagally mediated (not very likely), it´s most likely induced by chronic airway disease. Still, I would – and I forgot to mention that – check the E-lytes to exclude hyperkalemia.
Re the diastolic regurgitation: This is frequently seen in patients with marked bradycardia and has functional reasons (increased preload, lateral and apical displacement of papillary muscles).
Re ECG – I think, a 3-lead will do but 6 to 12 leads are certainly more accurate. I don´t know how many leads the cardiopet records – it´s not available in Austria 🙂
P

I’ve seen cases like this and
I’ve seen cases like this and I usually treat more aggressively respiratory and a little cardiac like sid lasix and acei just in case it will help. With mild volume overload I don’t think it will hurt but a theophyline doxycycline trial may help as well. Otherwise bronchoscopy. I guess this is “thoracic blanket” treatment but whatever makes him stop coughing the owners will be happy and not call you in the middle of the night. A good slug of hycodan 1 hour before bedtime will help the cough and sleep during the night as well.

Peter
Why would you
Peter
Why would you recommend spironolactone vs furosemide?

Eric you’re right, sometimes we just need to get the patient to stop coughing to make the owner happy. We have discussed bronchoscopy and TTA. This would be a referral procedure and a couple of hours away. The owners are not keen on this unfortunately. I have attempted a wash on my own in the past without the aid of a scope and the results were less than satisfying so I think they really need to be scoped to make it worth while.

The pet is coming in for a recheck tomorrow so will get an ECG!
Jacquie

I have inserted an ECG strip
I have inserted an ECG strip in the original post that I ran on my Cardell today but am waiting results from Cardiopet with atropine response test.

At recheck, the patient’s cough has improved further but still some throat sensitivity. I have added theophylline and will continue with a weaning course of pred – so some hope yet.

Heart rate does seem very low for a dog that seems anxious in the hospital.

Jacquie

And K+ is normal – only mild
And K+ is normal – only mild elevations in ALP and UREA.

Did you post both the pre-and
Did you post both the pre-and post atropine ECG strip? Heart rate is slow and if does not respond to to atropine then a primary myocardial conduction problem and heading towards possible pacemaker.

Respiratory disease can cause vagal inhibition and thus slowish heart rate. Also tends to go against cardiac disease as that should result in tachycardia.

Hi Remo, the above strip is
Hi Remo, the above strip is just a pre atropine ECG. But I do now have the results from the post atropine test (evaluated by a cardiologist) that indicates the presence of complete heart block, third-degree and need for a pacemaker in this patient. She failed the atropine response test.

So overall, a very interesting case. I doubt the owners are going to go for a pacemaker at this stage so we are going to concentrate on controlling the cough and I have discussed signs of cardiogenic shock with the owners.

I realize that this is an old
I realize that this is an old post but am wondering why pro-BNP was not mentioned as a way of differentiating between respiratory and cardiac cough for this patient.

Good point but I still trust
Good point but I still trust the la/ao ratio better than bnp but that’s just me.

Can be used but as Eric
Can be used but as Eric mentioned La/Ao ratio can be better.
Measurement of BNP is useful in establishing and/or excluding CHF in dogs with cough or dyspnea. Thus if there is only respiratory or cardiac disease then BNP is good but a potential problem is the patient with both disease simultaneously, which determining BNP is not that clear-cut.

I tend to use pro-BNP testing
I tend to use pro-BNP testing when owners won’t let me do anything else (bronze plan when working up a coughing patient) but have been running them less since I have echocardiography at my disposal.

This case is driving me crazy however and maybe I should consider running one! Have resorted to a trial of heart meds along with pred and theophylline. Will see how that goes.

Problem is that if you´re
Problem is that if you´re having respiratory disease causing some degree of pulmonary hypertension, then your NT-proBNP will be markedly increased in the absence of CHF. (I had tons of dogs with severely increase NT-proBNP who were not in CHF.) Additionally, since the patient has additional atrial standstill (don´t see p-waves), there will be increased diastolic filling. This could have an additional effect on NT-proBNP. Summarizing, these were the reasons why I did not recommend BNP initially.
My opinion is that this biomarker can give you some additional information but can currently not replace ultrasound/radiography.
Would be interesting how high it is here, but pls don´t expect too much…
Peter

Very good information to have
Very good information to have about the NT-proBNP test Peter. Thanks!