Download Cardiac Arrhythmias and Their Effect on Performance

AAEP FOCUS ON POOR PERFORMANCE PROCEEDINGS / 2015
Cardiac Arrhythmias and Their Effect on
Performance in Horses
Sophy A. Jesty, DVM, DACVIM
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Take Home Message—Arrhythmias can be identified on ECG
because of abnormal complexes or because of abnormal rhythm or
timing. Life threatening arrhythmias include extreme
tachycardias and extreme bradycardias. Performance limiting
arrhythmias include tachycardias, bradycardias, atrial fibrillation
and perhaps atrial premature complexes (APCs) and ventricular
premature complexes (VPCs). The most common treatments for
arrhythmias are rest +/- corticosteroids, and antiarrhythmic
drugs. Issues of safety should be considered in addition to issues of
performance.
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Author’s email—[email protected].
I. INTRODUCTION
Sinus rhythms are the heart’s opportunity to be physiologic; the
sinus node decides rate on a beat to beat basis. Most rhythms
are sinus and therefore you should assume the rhythm is sinus
unless there is a good reason to think otherwise (such as
abnormal timing or morphology). Generally speaking, sinus
rhythms don’t require treatment. If we treat the underlying
cause of sinus tachycardias or sinus bradycardias, the heart rate
will normalize as the underlying problem resolves.
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linicians tend to fear arrhythmias, and therefore might feel
unprepared to workup arrhythmias. With an understanding
of electrocardiogram (ECG) interpretation, a rhythm diagnosis
can usually be reached. Once the arrhythmia has been
identified, there are a few things to consider:
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Assess the quality of the ECG. Check the calibration
amplitude and paper speed. Look for artifacts.
Calculate the heart rate. Establish whether it is slow,
normal, or fast and whether it is variable.
Assess the overall rhythm. Establish whether changes
in rhythm are intermittent or persistent.
Assess each complex in turn. Establish whether all the
complexes are similar or not.
Examine the relationship between complexes. Check
whether each P wave has a QRS complex, and whether
each QRS complex is preceded by a P wave. Once
these steps have been completed, define the heart rate
and rhythm and construct a plan for further diagnostics
or treatment if necessary.
whether it requires therapy,
whether it’s related to underlying disease,
whether it might affect performance, and
whether it might affect safety.
II. ECG
The ECG is the only means to fully characterize rate and
rhythm. Remember that the ECG shows only the heart’s
electrical activity, not the mechanical activity. Occasionally,
electrical and mechanical activity are not associated (pulseless
electrical activity, e.g.). The standard paper speed is 25 mm/sec
and the standard sensitivity is 10 mm/mV, but these should be
changed if it would help interpretation. For example, increase
paper speed when assessing tachycardias to spread out all the
complexes, and increase sensitivity when assessing low voltage
complexes to make the complexes taller.
The P wave reflects atrial depolarization. If atrial depolarization
doesn’t start in the sinus node, the timing and morphology of
the P wave will be abnormal. The PR interval reflects the time
for AV node conduction. If the P wave does isn’t followed by a
QRS complex, the impulse was blocked at the AV node. The
Interpretation of the ECG should be systemic and logical… take
your time regardless of the situation. This will increase the odds
of a correct initial diagnosis, which will allow for the best
course of treatment. The following are steps to consider:
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AAEP FOCUS ON POOR PERFORMANCE PROCEEDINGS / 2015
QRS complex reflects ventricular depolarization. If ventricular
depolarization is not initiated by an impulse crossing the AV
node, the timing and morphology of the QRS complex will be
abnormal. Because normally the ventricles are driven by atrial
depolarization, every P wave should be followed by a QRS
complex, and every QRS complex should be preceded by a P
wave. If the P wave is not followed by a QRS complex, atrial
depolarization did not result in ventricular depolarization – the
impulse was blocked at the AV node. If a QRS complex is not
preceded by a P wave, ventricular depolarization did not result
from atrial depolarization, it was initiated from a site below the
atria (usually the ventricles). If there are complexes with
abnormal timing or morphology, ectopy (rhythm originating
from somewhere other than the sinus node) should be
considered. If ectopy is supraventricular (arising from above the
ventricles), there should be an associated P wave and the QRS
complex should be normal. If ectopy is ventricular, there will
be no associated P wave and the QRS complex should be
abnormal.
sodium channel blockers and potassium channel blockers, but
can also be treated with β-blockers. Antiarrhythmic drugs to be
used for VT include lidocaine, MgSO4-, procainamide,
phenytoin, amiodarone, sotalol, propranolol and quinidine.
SVT can be recognized by its fast rate, usually regular rhythm
(rapid atrial fibrillation is an exception), and normal QRS
complexes and associated P waves. Sometimes during
tachycardia, the P wave will be hidden in the preceding T wave.
SVT is best treated using some sodium channel blockers or
potassium channel blockers, but can also be managed using βblockers, calcium channel blockers, and digoxin.
Antiarrhythmic drugs to be used for SVT include MgSO4-,
procainamide, diltiazem, amiodarone, digoxin, propranolol,
verapamil, and quinidine.
Sodium channel blockers:
An ECG should be obtained whenever you are concerned about
rate and/or rhythm on a physical exam: inappropriate
bradycardia, inappropriate tachycardia, irregular rhythms that
don’t sound like physiologic 2° AV block, and in any horse that
has clinical signs referable to an arrhythmia including poor
performance.
III. ARRHYTHMIAS
Arrhythmias that require treatment include: 1.both life
threatening arrhythmias (tachycardias such as ventricular
tachycardia [VT] and supraventricular tachycardia [SVT], and
bradycardias such as 3° AV block) and, 2. performance
threatening arrhythmias (atrial fibrillation and atrial premature
complexes (APCs) or ventricular premature complexes (VPCs).
Pharmacokinetic and/ or pharmacodynamic information has
been published for quinidine, procainamide, lidocaine and
phenytoin in horses. Bioavailability of phenytoin after oral
administration can be variable.
IV. TACHYCARDIAS
Treatment of tachycardias is with antiarrhythmics drugs, but
antiarrhythmic drugs can be dangerous and the decision to use
them must be an informed one. Criteria for antiarrhythmic drug
use include a sustained heart rate > 100-120bpm, polymorphic
ventricular arrhythmias, R-on-T phenomena, and clinical signs.
β -blockers:
VT can be recognized by its fast rate, usually regular rhythm (if
the QRS complexes are monomorphic), and the abnormal QRS
complexes without associated P waves. VT is best treated using
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Pharmacokinetic and/ or pharmacodynamic information has
been published for propranolol in horses. This information is
not available for esmolol and atenolol, although both have been
used in horses with anecdotally good effect. Esmolol would be
prohibitively expensive for some owners.
AAEP FOCUS ON POOR PERFORMANCE PROCEEDINGS / 2015
Potassium channel blockers:
VI. ATRIAL FIBRILLATION
Atrial fibrillation (AF) is the most common clinically important
arrhythmia in horses. The prevalence is ~0.5%, but this
increases 5x in slow finishing racehorses. In >90% of cases of
AF in racehorses, the rhythm converts back to sinus rhythm
without any intervention. For this reason, you shouldn’t treat
AF that has developed within the last 48 hours; you should wait
to see if it converts by itself.
Pharmacokinetic and/or pharmacodynamic information has
been published for amiodarone in horses. This information is
not yet available for sotalol, but this study is underway.
The characteristics of AF on ECG include: 1. lack of
discernable P waves, 2. Fibrillation waves, 3. irregularly
irregular R-R intervals, and 4. Normal QRS morphology.
Calcium channel blocker:
About half of horses with AF have underlying heart disease
(usually valve regurgitations). Horses with longer duration AF
have a higher chance of not cardioverting and have a higher risk
of recurrence if sinus rhythm is restored. The most common
presenting concern is exercise intolerance/poor performance.
Predispositions for AF include large atria, high vagal tone, and
hypokalemia (such as with furosemide use). The most likely
trigger for AF is an APC. Horses in AF compensate for the
decreased
stroke volume by increasing heart rate, which is why
horses that need to work at HRmax cannot perform in AF – they
will require cardioversion to be able to work at their previous
level.
Pharmacokinetic and/or pharmacodynamic information has
been published for diltiazem in horses.
Other antiarrhythmic drugs:
Quinidine is by far the most commonly used antiarrhythmic
drug for cardioversion of AF, as it is fairly effective at ~85%.
Adverse effects are common, including widening of the QRS
complex, upper respiratory tract stridor, ataxia, tachycardia,
hypotension, diarrhea, and colic. Widening of the QRS
complex, upper respiratory tract stridor and ataxia are all signs
of quinidine toxicity; if they are noted, the dose should be
decreased or the drug should be discontinued. Quinidine’s
narrow margin of safety has fueled the search for an alternative
antiarrhythmic drug. Ideally such a drug would be readily
available, inexpensive, easy to administer, and effective with
few adverse effects. Flecainide, propafenone and amiodarone
are the 3 antiarrhythmic drugs most studied for cardioversion of
Pharmacokinetic and/or pharmacodynamic information has AF in horses. Flecainide and propafenone are ineffective for
been published for digoxin in horses. This information is not this purpose. Amiodarone is effective in ~50% of cases, but
available for MgSo4-, although it has been used in horses with cumulative dosing can result in prolonged diarrhea.
excellent effect.
In 2003, the first report of transvenous electrical cardioversion
(TVEC) was published. Two pacing catheters are placed via
jugular vein access; one is advanced into the pulmonary artery
and one into the right atrium. Positioning is confirmed on echo
and thoracic radiographs. The horse is anesthetized and the
pacing leads are hooked to a defibrillator. After synchronization
with the R wave is confirmed, the first shock is delivered (50100J). If this is unsuccessful, the joules can be incrementally
increased and/or the catheters can be repositioned. The success
rate is >95%, and there is no relationship between duration of
AF and likelihood of cardioversion. TVEC does not increase
troponin to a serious degree, so it doesn’t appear to damage the
myocardium. Placement of the catheters affects the energy
V. BRADYCARDIAS
High 2° AV block and 3° AV block can be recognized by the
multitude of P waves not followed by QRS complexes and the
presence of escape complexes. Traditionally, AV node
dysfunction in horses has been treated with corticosteroids, but
this might be ineffective if significant fibrosis of the node has
occurred. Pacemaker implantation can be performed in horses,
but I would never consider them safe to ride. If pacemaker
implantation is impossible, positive chronotropes can be tried
(aminophylline, hyoscyamine, propantheline).
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AAEP FOCUS ON POOR PERFORMANCE PROCEEDINGS / 2015
required for cardioversion. Despite the benefits, TVEC will
never replace quinidine because of its relative unavailability
and the need for specialized equipment and expertise.
Nonetheless, it remains an excellent alternative to treatment
with quinidine in certain cases, especially given its extremely
high success rate.
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VII. APCS/ VPCS
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The question of how dramatically APCs and VPCs affect
performance remains unanswered. Early complexes do
decrease cardiac output for that beat, so if the horse is
performing at the highest levels, early complexes likely do
contribute to poor performance. However, there are a number
of papers documenting APCs and VPCs in horses without poor
performance, making their significance difficult to understand.
Depending on the study, the prevalence of APCs during
exercise ranges from 0-89% and the prevalence of VPCs ranges
from 0-18%. Exercising arrhythmias seen in horses performing
normally are not associated with heart size or valve
regurgitations and troponin is normal. But regardless of
performance, the presence of APCs predisposes to the
development of atrial fibrillation and the presence of VPCs
predisposes to the development of ventricular fibrillation,
which will cause sudden cardiac death. For this reason, the
presence of anything more than a single VPC during exercise
prompts me to consider the horse unsafe to ride until those
arrhythmias have resolved.
5.
Once a good sinus tachycardia develops, the rhythm
should be regular, especially once HRmax is reached.
APCs and VPCs are recognized based mostly on the
interruption of the underlying rhythm. Specific
classification is based on QRS morphology and the
absence or presence of a compensatory pause. I do not
consider VPCs safe during peak exercise.
Single APCs and VPCs are acceptable during the postexercise period when both sympathetic tone and
parasympathetic tone are elevated. Sometimes also during
this period, unusual manifestations of surges in vagal tone
are apparent (‘early’ AV block, sinus arrhythmia).
Heart rate recovery should be fast; I expect the heart rate
to drop to <100 bpm by 120 seconds after exercise.
If a horse has even mild arrhythmias during peak exercise, I
recommend rest for 30-60 days with hand walking only, and a
tapering course of corticosteroids: dexamethasone at 30 mg q
24 for 3 days, 20 mg q 24 h for 3 days, 10 mg q 2 4h for 3 days,
10 mg EOD for 3 treatments. ACKNOWLEDGMENTS
Declaration of Ethics
The Author declares that she has adhered to the Principles of
Veterinary Medical Ethics of the AVMA.
Conflicts of Interest
A paper reported on the cause of sudden cardiac death in 5
racehorses immediately after intense exercise and speculated it
was due to arrhythmias. One horse had an ECG to document
this; the others didn’t have an ECG but all had regions of
fibrosis in the conduction system, which could have
predisposed to arrhythmias. Another paper reported the cause
of death of racehorses and postulated that heart disease was not
a common cause. However, arrhythmias might be ‘silent’ on
necropsy. Even more confounding is the fact that interobserver
agreement for the identification of arrhythmias in exercising
horses is poor (although experience increased agreement). The
most valid means to differentiate an APC from a VPC is that
the APC should have a normal QRS and no compensatory
pause, while the VPC should have an abnormal QRS and a
compensatory pause. The presence of AF causes even greater
difficulty for arrhythmia identification. This is for 2 reasons: the
heart rate is much higher in horses with AF for a given level of
exercise, which makes ECG analysis more difficult, and the
underlying irregularity of the rhythm makes the assessment of
a complex as early tricky. In addition, with an irregular rhythm
the ventricular conduction system might be caught off guard
with the arrival or an early complex and the QRS might appear
wide and bizarre despite a supraventricular origin.
The Author has no conflicts of interest to disclose.
My own assessment of the stress ECG includes the following:
1.
The time to HRmax shouldn’t be immediate, but should
steadily increase as exercise increases. If HRmax is
reached too quickly, it’s compensating for something else.
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