LilianaLove
Boxer Pal
Hi all. I don't have a boxer, but I do have a lovely little pit bull who is going to need a holter monitor soon. I'm a vet tech, but I've never used one of these, have no experience with them, and I don't know how she'll handle it.
For the full story, continue reading, for the question, skip to the bottom:
Background information: Lily was diagnosed with hypoaldosteronemia (a very rare for of Addisons, in which the body produces normal cortisol levels but does not produce enough aldosterone) in July of this year (she is 3 years old).
I brought Lily in for routine bloodwork on friday to check her electrolytes and kidney values. We increased her Florinef to 1.75 tablets BID (0.35mg total daily).
By chance, I decided to recheck her heart rate and BP, for monitoring purposes. When I listened to her heart, I couldn't even discern a heart rate. There was so much fluttering and missing beats it was incomprehensible. So I hooked her up to the EKG and it showed tachycardia.
My boss initially attempted to treat the tachycardia with ateno
, which did not seem to work. We then tried IV atropine, which did work to resolve the heart block we were seeing. We had assumed the tachycardia was ok, since that is what atropine is for, speeding up the heart rate. The next day, we were still seeing heart block, though we were using very low dose atropine.
After attempting to monitor and treat her for 2 days, I had to take her to the ER, as my boss was unavailable for communication and I needed help (and sleep). The ER did nothing more than monitor, which was fine, as she had a cardiology consult in the morning (monday morning).
The cardiologist did an echocardiogram, EKG, and BP. The cardiologist discerned that the heart block was a result of the tachycardia, and that what we needed to be doing was slowing down her heart rate, not speeding it back up. We initially did not understand why she was saying this, as when we tested with atropine, it resolved the block.
The bottom line is Lily WAS in heart block. The cardiologist was, however, correct that the heart block was physiological. Lily was in atrial tachycardia, meaning the SA node (the electrical impulse telling the atrium to contract) was firing too rapidly and causing too many atrial contractions. When measured on EKG, Lily's heart rate was actually around 300bpm (her normal resting HR is 80bpm, tachycardia is considered anything over 180bpm). The heart block was caused by the fact that the atrium was contracting more rapidly than the ventricle's refractory period. So, the atrium was contracting, but the ventricle did not have enough blood in it to warrant contracting, so the ventricle did not contract, leaving the EKG reading P waves without QRS complexes (heart block) and subsequent pulse deficits. So it looked like she was in heart block when, in reality, her ventricle was being smart and not over working itself. This is still considered heart block, but tachycardic type II 2nd degree. So, when we gave the atropine, it only seemed like we were getting rid of the block, and solving what we thought was the problem, however we were artificially stimulating the ventricle to contract, thus every P then had a QRS and a pulse for every beat.
At the cardiologist, probably due to stress and heart exhaustion, she had episodes of ventricular tachycardia and ventricular premature contractions (VPCs). Had this progressed, she could have possibly gone into cardiac arrest. However, her body once again compensated and attempted to slow her heart rate.
She is currently on a medication, Sota, an anti-arrhythmic, so slow down her heart rate and stop the atrial tachycardia.
We will be rechecking an EKG next week, and the week after she will have Holter monitor to assure the sota is doing what it's supposed to be doing and that her heart remains in normal rhythm.
There are a lot of things that don't make sense with her- the fact that she entered true, 2nd degree heart block at one point on sunday and the fact that she exhibited v-tach and VPCs only once and recovered fine. Unfortunately, I ran out of EKG paper sunday morning and had to simply record video and take pictures, so I can't measure the P waves from the time on sunday that her heart rate slowed down significantly and she exhibited true heart block. However, I do know that the block she was exhibiting at that time had nothing to do with any current state of tachycardia, I just can't prove it on EKG.
I've already sent out a full tick panel PCR, include lyme disease C6, screening to rule out tick-borne illness as a cause of any myocarditis. We are researching the necessity of running a Troponin I level.
We are still very much of the belief that this is a reaction to the increased dose of medication, as she had a similar reaction at 2 tablets BID.
There is a chance she may need to stay on the sota if we have any hope of getting her back on the florinef. We can't keep her off the florinef; she will inevitably go into kidney failure. So my boss will talk to the internal medicine specialist and the other cardiologist and see if we can get a full-body approach to our treatment plan. For now, until her arrhythmias stop, she will be off the florinef, meaning I'll have to add water to her diet on a regular basis again, basically every few hours like before.
I came to a boxer forum because my understanding is that boxers are routinely tested with holter monitors and someone might have some insight.Lily is very 'anti-harness' and I don't know how she will handle it. She will have to wear it for 2-4 weeks.
Thanks for reading and for any suggestions.
For the full story, continue reading, for the question, skip to the bottom:
Background information: Lily was diagnosed with hypoaldosteronemia (a very rare for of Addisons, in which the body produces normal cortisol levels but does not produce enough aldosterone) in July of this year (she is 3 years old).
I brought Lily in for routine bloodwork on friday to check her electrolytes and kidney values. We increased her Florinef to 1.75 tablets BID (0.35mg total daily).
By chance, I decided to recheck her heart rate and BP, for monitoring purposes. When I listened to her heart, I couldn't even discern a heart rate. There was so much fluttering and missing beats it was incomprehensible. So I hooked her up to the EKG and it showed tachycardia.
My boss initially attempted to treat the tachycardia with ateno
, which did not seem to work. We then tried IV atropine, which did work to resolve the heart block we were seeing. We had assumed the tachycardia was ok, since that is what atropine is for, speeding up the heart rate. The next day, we were still seeing heart block, though we were using very low dose atropine. After attempting to monitor and treat her for 2 days, I had to take her to the ER, as my boss was unavailable for communication and I needed help (and sleep). The ER did nothing more than monitor, which was fine, as she had a cardiology consult in the morning (monday morning).
The cardiologist did an echocardiogram, EKG, and BP. The cardiologist discerned that the heart block was a result of the tachycardia, and that what we needed to be doing was slowing down her heart rate, not speeding it back up. We initially did not understand why she was saying this, as when we tested with atropine, it resolved the block.
The bottom line is Lily WAS in heart block. The cardiologist was, however, correct that the heart block was physiological. Lily was in atrial tachycardia, meaning the SA node (the electrical impulse telling the atrium to contract) was firing too rapidly and causing too many atrial contractions. When measured on EKG, Lily's heart rate was actually around 300bpm (her normal resting HR is 80bpm, tachycardia is considered anything over 180bpm). The heart block was caused by the fact that the atrium was contracting more rapidly than the ventricle's refractory period. So, the atrium was contracting, but the ventricle did not have enough blood in it to warrant contracting, so the ventricle did not contract, leaving the EKG reading P waves without QRS complexes (heart block) and subsequent pulse deficits. So it looked like she was in heart block when, in reality, her ventricle was being smart and not over working itself. This is still considered heart block, but tachycardic type II 2nd degree. So, when we gave the atropine, it only seemed like we were getting rid of the block, and solving what we thought was the problem, however we were artificially stimulating the ventricle to contract, thus every P then had a QRS and a pulse for every beat.
At the cardiologist, probably due to stress and heart exhaustion, she had episodes of ventricular tachycardia and ventricular premature contractions (VPCs). Had this progressed, she could have possibly gone into cardiac arrest. However, her body once again compensated and attempted to slow her heart rate.
She is currently on a medication, Sota
, an anti-arrhythmic, so slow down her heart rate and stop the atrial tachycardia. We will be rechecking an EKG next week, and the week after she will have Holter monitor to assure the sota
is doing what it's supposed to be doing and that her heart remains in normal rhythm. There are a lot of things that don't make sense with her- the fact that she entered true, 2nd degree heart block at one point on sunday and the fact that she exhibited v-tach and VPCs only once and recovered fine. Unfortunately, I ran out of EKG paper sunday morning and had to simply record video and take pictures, so I can't measure the P waves from the time on sunday that her heart rate slowed down significantly and she exhibited true heart block. However, I do know that the block she was exhibiting at that time had nothing to do with any current state of tachycardia, I just can't prove it on EKG.
I've already sent out a full tick panel PCR, include lyme disease C6, screening to rule out tick-borne illness as a cause of any myocarditis. We are researching the necessity of running a Troponin I level.
We are still very much of the belief that this is a reaction to the increased dose of medication, as she had a similar reaction at 2 tablets BID.
There is a chance she may need to stay on the sota
if we have any hope of getting her back on the florinef. We can't keep her off the florinef; she will inevitably go into kidney failure. So my boss will talk to the internal medicine specialist and the other cardiologist and see if we can get a full-body approach to our treatment plan. For now, until her arrhythmias stop, she will be off the florinef, meaning I'll have to add water to her diet on a regular basis again, basically every few hours like before.I came to a boxer forum because my understanding is that boxers are routinely tested with holter monitors and someone might have some insight.Lily is very 'anti-harness' and I don't know how she will handle it. She will have to wear it for 2-4 weeks.
Thanks for reading and for any suggestions.
