– 6 year old FS DSH acute onset of dyspnea and open-mouth breathing- referring vet gave furosemide prior to referral
– chest rads consistent with pulmonary edema and bloodwork unremarkable
– echo showed normal IVS and PW thickness in diastole when measured (<6mm)
– LAE is present and trace pericardial effusion
– I think there is SAM on colour flow (do you agree?)
– aortic max velocity 2.27 m/s
– what is causing the CHF if the LV walls are wnl? the basilar region of the IVS looks thick to me? a basilar form of HCM?
– 6 year old FS DSH acute onset of dyspnea and open-mouth breathing- referring vet gave furosemide prior to referral
– chest rads consistent with pulmonary edema and bloodwork unremarkable
– echo showed normal IVS and PW thickness in diastole when measured (<6mm)
– LAE is present and trace pericardial effusion
– I think there is SAM on colour flow (do you agree?)
– aortic max velocity 2.27 m/s
– what is causing the CHF if the LV walls are wnl? the basilar region of the IVS looks thick to me? a basilar form of HCM?
– we have started furosemide therapy and have discussed other heart meds with the client (fortekor, plavix)
Thanks for your help!
Comments
Dear Jacquie!
I totally
Dear Jacquie!
I totally agree. This cat is in CHF and has SAM. I cannot make measurements on this but I still see that the basal septum and the papillaries are hypertrophied. That’s why advanced HCM is possible. The differential to this would be UCM or RCM. Both can cause CHF without LV hypertrophy. The pericardial effusion here is due to CHF as well.
The color clip is very nice, Jacquie!!
I woudl start with Furosemid as you already did (e.g. 0.5-1 mg/kg/hr or 2 mg/kg q 3-4 hrs until the edema resolves, followed by an oral dosage of 2 mg/kg bid). Anticoagulants are as well indicated. I usually prefer Heparin while the patients are hospitalized and go for Plavix once they go home. An ACEI is indicated once pilling is possible without harm to the patient (once the pulmonary edema has at least almost resolved) and if the blood pressure is over 120 mm Hg (systolic).
If concomitant hypertension or hyperthyroidism are noted, this has to be treated appropriately.
Best regards from New Jersey!
Peter
Dear Jacquie!
I totally
Dear Jacquie!
I totally agree. This cat is in CHF and has SAM. I cannot make measurements on this but I still see that the basal septum and the papillaries are hypertrophied. That’s why advanced HCM is possible. The differential to this would be UCM or RCM. Both can cause CHF without LV hypertrophy. The pericardial effusion here is due to CHF as well.
The color clip is very nice, Jacquie!!
I woudl start with Furosemid as you already did (e.g. 0.5-1 mg/kg/hr or 2 mg/kg q 3-4 hrs until the edema resolves, followed by an oral dosage of 2 mg/kg bid). Anticoagulants are as well indicated. I usually prefer Heparin while the patients are hospitalized and go for Plavix once they go home. An ACEI is indicated once pilling is possible without harm to the patient (once the pulmonary edema has at least almost resolved) and if the blood pressure is over 120 mm Hg (systolic).
If concomitant hypertension or hyperthyroidism are noted, this has to be treated appropriately.
Best regards from New Jersey!
Peter
Once a cat is already in CHF,
Once a cat is already in CHF, how important is it to know if it is HCM vs RCM? Is it purely academic at this stage as treatment is the same?
Hope you are enjoying your North American tour!
Jacquie
Once a cat is already in CHF,
Once a cat is already in CHF, how important is it to know if it is HCM vs RCM? Is it purely academic at this stage as treatment is the same?
Hope you are enjoying your North American tour!
Jacquie
Does not make any difference,
Does not make any difference, Jacquie. It is purely academic. Only thing is not monitor because once systolic dysfunction develops (low FS, maybe <30), I would add pimo ad 1/2 dog dosage
thanks, had 2 great days in NJ, thanks to Eric! Just on airport heading for Austria
Was great to meet you!
Peter
Does not make any difference,
Does not make any difference, Jacquie. It is purely academic. Only thing is not monitor because once systolic dysfunction develops (low FS, maybe <30), I would add pimo ad 1/2 dog dosage
thanks, had 2 great days in NJ, thanks to Eric! Just on airport heading for Austria
Was great to meet you!
Peter
I just say CHF with
I just say CHF with cardiomyopathy because things change once they stabilize regarding categories…. may look like UCM when failing and then when stable the LV measures thick or technically so. Sometimes I think we just fool ourselves thinking we can put cat hearts in an academic box of naming…cats are aliens and just like infectious disease and “doxycycline responsive disease” vs a 4dx test or lepto titer…. feline cmy is a bit more complicated than a few names we try to categorize them in.
In this case I find the SAM relevant, the septal fixed obstruction with the ivs “hook” and the papillary hypertrophy and of course the volume overload and your pretty colors. I would name this “segmental hcm with fixed and dynamic obstruction and left chf” but I am feeling poetic today:)
Thanks to me JP??? I had lots of help in all aspects of the conference thats for sure:)
Great post
I just say CHF with
I just say CHF with cardiomyopathy because things change once they stabilize regarding categories…. may look like UCM when failing and then when stable the LV measures thick or technically so. Sometimes I think we just fool ourselves thinking we can put cat hearts in an academic box of naming…cats are aliens and just like infectious disease and “doxycycline responsive disease” vs a 4dx test or lepto titer…. feline cmy is a bit more complicated than a few names we try to categorize them in.
In this case I find the SAM relevant, the septal fixed obstruction with the ivs “hook” and the papillary hypertrophy and of course the volume overload and your pretty colors. I would name this “segmental hcm with fixed and dynamic obstruction and left chf” but I am feeling poetic today:)
Thanks to me JP??? I had lots of help in all aspects of the conference thats for sure:)
Great post
I know this is an older post
I know this is an older post but I am a newbie (to echos) and just going through the forum. The second cine loop cofuses me a bit. I see the SAM and dilated L atrium. Is that focal basilar hypertrophy of the IVS pressing into the aortic outflow tract? If that is IVS then what is the chamber noted between the IVS and L ventricle? It seems to attach to the basilar hypertrophy. I hope I am clear in my question.
I know this is an older post
I know this is an older post but I am a newbie (to echos) and just going through the forum. The second cine loop cofuses me a bit. I see the SAM and dilated L atrium. Is that focal basilar hypertrophy of the IVS pressing into the aortic outflow tract? If that is IVS then what is the chamber noted between the IVS and L ventricle? It seems to attach to the basilar hypertrophy. I hope I am clear in my question.
Hi!
Yes, its basal
Hi!
Yes, its basal hypertrophy. Dynamic left ventricular outflow tract obstruction mostly comprises SAM and basal hypertrophy. Both are present here. There’s a huge papillary muscle coming into view in systole, but I don’t think it’s directly attached to the septum. There’s just a so called false tendon originating from that papillary muscle and ending at the basal septum. That’s why the hyperechoic part of the basal septum is sometimes referred to as traction lesion. Short axis and apical views woudl probably help understanding the exact morphology in this case.
Does this answer your question?
Best regards and thanks for posting!
Peter
Thank you Peter – this did
Thank you Peter – this did answer my question. I thought that may be the case but I was not sure.
Hi!
Yes, its basal
Hi!
Yes, its basal hypertrophy. Dynamic left ventricular outflow tract obstruction mostly comprises SAM and basal hypertrophy. Both are present here. There’s a huge papillary muscle coming into view in systole, but I don’t think it’s directly attached to the septum. There’s just a so called false tendon originating from that papillary muscle and ending at the basal septum. That’s why the hyperechoic part of the basal septum is sometimes referred to as traction lesion. Short axis and apical views woudl probably help understanding the exact morphology in this case.
Does this answer your question?
Best regards and thanks for posting!
Peter
Thank you Peter – this did
Thank you Peter – this did answer my question. I thought that may be the case but I was not sure.
Peter is a “traction lesion”
Peter is a “traction lesion” the same as a “jet lesion?”
Peter is a “traction lesion”
Peter is a “traction lesion” the same as a “jet lesion?”