CC – Abby Answer!
| March 16, 2013 | Posted by Melinda under Uncategorized |
And the answer to this week’s CC is……Atrial Fibrillation!
Congratulations to Dom who was at the writing of this post, the only commentor. Dom got very close to the answer because they identified it as an “arrhythmia” and pointed to low Potassium as a possible contributor.
What is A fib?
There are 2 phases in the heart cycle. During the filling phase, the heart is filling with blood – blood passes through the atrium (top part of the heart), through a one way valve into the ventricle (bottom part of the heart). When the heart contracts, the atrium contracts slightly before than the ventricle. The last bit of blood is squirted into the ventricle, and then the blood in the ventricle is pushed into the great vessels to the rest of the body.
A complex electrical system coordinates when the heart contracts. There is a natural “pacemaker” that is located near the atriums of the heart. This is the dominant pacemaker under normal situations, however there are other pacemakers in the heart that can take over if this dominant one becomes damaged, or with damage to the heart, cells can become abnormal and start to function as pacemakers.
The pacemaker gives electrical signals to the atrium when it’s time to contract, and then those signals travel to the ventricle (after expeiencing a slight delay as described earlier). Due to some physiological mechanisms that we are NOT going to go into here, there is a limit to how soon you can ask cells to contract right after a contraction ie there is a period after a cell contracts that matter how nicely you ask, it won’t contract again.
During A fib, this system gets all messed up. During a signal to contract, some cells in the atrium are ready and so contract, other cells are in that refractory period, and so don’t contract. If another signal comes right away to contract, the cells that were in the refractory period are now out of it, and do, but the other cells are now in the refractory period and don’t!!!!! This sets up a situation where some population of cells in the atrium are always excitable and ready to contract, meaning that some parts of the atrium can contract whenever a signal tells it to do so.
Now lets combine the scenerio where some cells in the heart are always ready to contract with another – an abnormal etopic pacemaker (ie some damaged heart cells have developed pacemaker abilities) or a normal pacemaker that has decided to abandon it’s orderly way of life. It pumps out a signal for cells to contract much more rapidly and since some population of atrial cells are always ready to contract……you get very rapid, uncoordinated contraction of the atrium. The atrium never relaxes or contracts properly.
What about the ventricle? There is a delay system that pauses signals that travel from the atrium to the ventricle, to make sure the atrium contracts slightly before the ventricle. Additionally, the ventricle is still normal in that all of it’s cells are excitable and refractory at the same time – it doesn’t matter if it’s getting a signal to contract really fast – the cells can only respond to that signal AFTER they are done with their refractory period.
So even though your atrium is going crazy, your ventricle is still managing to pump blood out to your body in a fairly coordinated fashion.
Which is fine until you try to exercise……..then that little bit of extra blood that the atrium normally pushes into the ventricle before the ventricle contracts becomes really important (not just because of the volume of blood but what it does to the stretching of the ventricle wall – a concept that is REALLY cool but that I won’t go into here)…..and without that the horse develops “exercise intolerance” which is the most common presenting complaint for a horse in A fib.
Who gets AF?
There are 3 classes of animals that get AF – those with heart disease (because like I mentioned, heart dz can damage heart cells and cause them to behave in weird ways like start acting like pacemakers, or disrupting the coordination of refractory and excitable phases in populations of cells), young to middle aged race horses with no heart failure disease with an acute (sudden onset) presentation of exercise intolerance, and middle-aged large thoroughbred (or crosses) with no heart failure disease, but a vague history of exercise intolerance.
Besides heart failure, other factors that can increase the chances of AF developing include some viral diseases, low potassium levels, anemia, colic etc.
Once the AF has started (ie – an event happens that causes the AF) it can persist (ie, NOT cure itself). Fun fact – in horses that are OVER 15 hands, the heart is large enough that once it gets started it will persist instead of reverting back to a normal rhythm. Bummer for large horses!!!!!!! Thus while it MIGHT be true that your little endurance horse who developed an AF during a ride because of an electrolyte inblanace might revert and be fine, be cautioned that your larger horse, OR your small endurance horse with underlying cardiac disease that results in an enlarged atrium (and don’t assume that just because you have a stellar athlete 100 mile horse that it doesn’t have cardiac disease) WILL NOT NECESSARILY REVERT. And may need to have treatment for it to do so.
What does AF look like?
Number one clinical sign is exercise intolerance. In the horse, the heart rate may be normal, or even below normal! As long as the filling phase of the heart cycle is long enough than you will get a quality pulse (ie blood being pumped in the body). The “R-R” (think of it as the time it takes to complete one heart cycle which = filling+pumping) will be variable – this “arrthymic”. The heart rhythm will be irregular – in contrast to some other conditions, the heart rate is irregularly irregular.
AF is different in horses than other animals. Horses have an ENORMOUS cardiac reserve, which means often AF and other heart issues are undetectable until you ask the horse for a large effort – like racing, polo etc.
Some more unusual presentations can include the horse becoming uncoordinated and collapsing during exercise. That sounds like intolerance to me!!!! But more likely the AF horse without heart disease is getting tired fast and doesn’t have the stamina, decreased recoveries etc.
My horse has AF – what now?
Successful treatment depends on whether there is underlying heart disease that is causing it, or if the AF has been going on for longer than 4 months (remember that if the heart is big enough – such as horses over 15 hands that an AF can’t correct itself once it gets going). These horses are more likely to have a relapse in the future, even if the initial treatment was successful.
In addition to a physical exam, a blood panal (to look at potassium levels etc.) and other heart tests such as an ECG and cardioultrasound (to look at whether the horse has underlying cardiac disease in addition to the AF) may be necessary.
Treatment is aimed at returning the heart to “sinus” (normal) rhythm. Oral (through a stomach tube) doses of quinidine sulfate is used….Doses are repeated every 2 hours until sinus rhythm is achieved or when toxic side effects are seen……Being a second year vet student, I am not as familiar with treatments as I am with physiology and mechanisms, so I’ll leave a detailed explanation to my reader’s google searches :).
Treatment is not without it’s risks and the decision of whether to treat depends on the precense of underlying heart disease. If AF is found as an incidental finding (which it often is) and has been there for a prolonged time and the horse is performing to satisfaction, it might not be worth it to treat. In acute onset AF in a horse showing exercise intolerance with no underlying heart disease? May be a good candidate to treat. Horses with AF “should not be used for arduous competition and the level of work for which they are used should not be increased from that of which they were previously known to be capable without tiring, unless treatment is successful”. (From Provet)
Prognosis
I took this information from Tufts vet school website.
In horses whose resting heart rate is less than 60 (Increased resting heart rate can indicate heart disease), and the AF has been present for less than 4 months, and there is no heart murmur (or a very minor one) –> prognosis is excellent (95%).
If any of the conditions are present in the previous paragraph…..prognosis is guarded to good (80% chance of reverting the AF to normal sinus rhythm, BUT 60% chance that the AF will return).
So what about Abby?
Let’s assume that Abby is a big girl over that 15 hand mark (she is a standardbred after all). She doesn’t show any other signs of heart disease, no murmurs were heard, and she falls into that category of young racehorses that acutely present with exercise intolerance. Based on this information, I think that she is a good candidate for treatment, with an excellent prognosis. Since low potassium is associated, perhaps suggest that Abby’s owner do some research into electrolyte replacement both before, at, and after the ride that will help Abby keep her electroytes balanced. If Abby’s owner is secretly using Lasix ( a loop diuretic that causes potassium loss and is used in race horses to control “bleeders”)…..than that should be discontinued!
I recognized this because it’s almost exactly what happened to Ozzy in Maryland. He just suddenly got tired on me out there (it was warmer than usual for that time of year). At the vet check his heart rate was up and down, but not in any rhythmic was. We got the EKG on him. He has a sinus arrhythmia. We got bloodwork, etc. done on him. He needs careful monitoring, especially during heavy work, and I have to give him extra K before/during/after endurance rides. However, it wasn’t a career ender and my vet assured me that he’s not likely to just drop dead from it one day. Still a scary diagnosis to go through. For what it’s worth, your description of the events was so spot on that I was wondering if you were talking about Ozzy! (he’s a standardbred and everything)
Dom – What’s funny is after I posted this, I started panicking – what if what I posted isn’t a typical presentation for this at all??????? I frantically had my best friend who is in school with me, whose mom is a horse vet, look it over and tell me if it was even reasonable. She assured it me was, but I was half way expecting a vet to come on and tell me how I got it all wrong LOL.
I specifically picked a standardbred because they seem to be a breed predisposed to getting this as young (under 10 years of age) fit racehorses with no underlying heart disease. I’m glad Ozzie is doing OK – That would not have been a fun diagnosis to go through even with the information I have know.
Dom – if you want to shoot me your address to my email at [email protected], I’ll mail you a little something for playing :).
As soon as I read Dom’s name in the comments, I remembered about Ozzy’s presentation with this.
Small world, considering we’re all relatively far apart. Ahhhh, standardbreds.