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Interpreting the equine ECG

Ruth Morgan MA VetMB CertAVP(EM) MRCVS
PHILLIP LEVERHULME LARGE ANIMAL HOSPITAL, UNIVERSITY OF LIVERPOOL, LEAHURST, NESTON,
SOUTH WIRRAL. CH64 7TE

ABSTRACT: Electrocardiography has many applications in equine practice. The identification of arrhythmias and
interpretation of their significance is frequently challenging. When interpreting the ECG trace the clinician is
faced with several important questions: What is the diagnosis, the potential clinical significance and, most
importantly, is the horse safe to ride? This article will try to present a logical approach to interpreting
electrocardiogram traces in the horse. DOI: 10.1111/j.2044-3862.2012.00185.x

INTRODUCTION Box 1 Interpreting the equine ECG trace

The ECG cannot be interpreted without a good
clinical history and a thorough clinical examination.
It is vital to know full details of the horse and the
circumstances in which the trace was obtained.
The ECG trace is the detection of the electrical
signal from the heart detected at the body surface.
(See previous article for discussion of the generation
of the trace and factors affecting it (Vol 17.4 10pp).)
The P wave represents atrial depolarisation, the QRS
represents ventricular depolarisation and the T wave
ventricular repolarisation. Using a base-apex lead
configuration, the P wave is normally a positive
deflection and the QRS a large negative deflection.
It is important that the P waves are clearly visible, as
this helps to determine the origin of any
dysrhythmia. The P wave can be biphasic or
notched, due to the large size of the atria. P wave
morphology may differ between complexes
(wandering pacemaker). The T wave is extremely
variable and can change even from beat to beat.
Little significance can be attached to changes in the
T wave of the horse.
The trace must be examined manually in detail. This
may take some time, particularly with 24-hour
traces, but unfortunately the algorithms used for
automatic analysis of small-animal traces are not
available for equine ECGs due to the variability in
the size and form of the QRS complex and
particularly the T wave. (See Box 1 for questions to
ask when interpreting the trace.)
EQUINE l CLINICAL HH
l Is the trace diagnostic, with minimal interference
and clear R-R intervals, allowing adequate
interpretation? Are the P waves visible? See
above for mechanisms to reduce interference.
l What is the heart rate?
l Is the rhythm regular or irregular? Is the
irregularity persistent throughout the trace or is
it intermittent?
l If it is irregular, is it regularly irregular or
irregularly irregular?
l Is there a P for every QRS?
l Is there a QRS for every P?
l Are the QRS configurations uniform in shape?
Is the trace diagnostic?
Identifying artefacts or a poor-quality trace is the
first step when assessing an ECG. Very little
significance can be given to changes detected on a
trace in which it is difficult to identify the ECG
complexes clearly. Horse movement and poor
electrical contact are the most common causes of
interference and it is worth spending time getting a
high-quality trace, as this will facilitate
interpretation. Interference can often be
distinguished from electrical cardiac activity by the
sharpness and rapidity of the deflection or a
wandering of the baseline (Fig. 1). If you do not feel
the trace is adequate, reposition the electrodes or try
to get better contact by clipping or applying more
alcohol to the area.

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Fig. 1: This trace is non-diagnostic due to interference.

4 Companion Animal Vol 17 June 2012 © 2012 Blackwell Publishing Ltd

INITIAL ASSESSMENT
Heart rate
Many modern ECG monitors will calculate heart
rate and display it alongside the trace. If not, it should
be calculated by counting the number of complexes
in a set time period, for example in 12 seconds.
Alternatively, 60 can be divided by the R-R interval
in seconds to give a rate. In the case of an exercising
ECG, the rate for different stages of the examination
should be determined, with particular attention
being paid to the maximum heart rate achieved. The
heart rate at rest is vital for assessing the significance
of any arrhythmia detected as it indicates how well
the heart is compensating.
Is the rhythm regular or irregular?
Visual assessment of the R-R intervals will allow the
clinician to determine if the rhythm is regular or
not. Take into account increases in heart rate due to
factors such as the horse becoming excited, as these
are often misinterpreted. If an irregularity is detected
it is important to determine whether or not the
irregularity occurs at regular intervals, i.e. is it
regularly irregular or is there no pattern to the
irregularity. It is often necessary to obtain a trace of
at least ten minutes and, if possible, longer to ensure
that subtle irregularities are not missed.
Is there a P wave for every QRS and
a QRS for every P wave?
The P wave represents atrial depolarisation and so its
presence or absence allows us to distinguish the
origin of arrhythmias. For example if the P wave is
present but it is not followed by a QRS then the
atria have depolarised but the electrical conduction
has been blocked at the atrio-ventricular node, i.e.
this is second-degree AV block.
What is the morphology of the QRS?
The QRS morphology differs between horses but
should be uniform in the same horse. The shape of
the QRS complex is determined by the very
uniform depolarisation of the ventricle, starting at
the AV node. If depolarisation of the ventricles starts
at a place other than the AV node, or follows a
different path, the QRS will often have an altered
morphology.
Fig. 2: A trace showing second-degree atrioventricular block.
© 2012 Blackwell Publishing Ltd
ARRHYTHMIAS
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Arrhythmias can be classified as bradyarrhythmias or
tachyarrhythmias, i.e. those occurring at slow or fast
heart rates. This classification can be misleading, as
premature depolarisations, for example, are often
called tachyarrhythmias but can occur when the
overall resting heart rate is normal. Alternatively,
arrhythmias can be classified as pathological or
physiological. Some physiological arrhythmias, such
as second-degree AV block, can be categorised
easily, but premature depolarisations can be
pathological or physiological depending on their
aetiology and thus confusion can arise. Arrhythmias
are also named according to their origin.
Supraventricular arrhythmias originate from the
atria, the atrioventricular node or the junctional
tissue, whereas ventricular arrhythmias originate
from ventricular tissue.
Second-degree atrioventricular block (AV block)
First-degree AV block refers to a delayed conduction
at the AV node but the electrical signal itself is not
blocked. Second-degree AV block refers to a block
of one or two sequential electrical impulses at the
AV node. This is the most commonly detected
arrhythmia in the horse (Raekallio et al., 1992). It
usually occurs at low or normal heart rates and is
thus usually classified as a bradyarrhythmia.
However, occasional second-degree AV block occurs
at raised heart rates in horses, for example following
surgery. Second-degree AV block is thought to arise
due to high vagal tone and is not usually of
pathological significance, hence it is generally
considered a physiological murmur. A P wave is
present but is not followed by a QRS complex.
Occasionally two sequential P waves are blocked.
Second-degree AV block should disappear with
exercise or excitement (Fig. 2).
Advanced atrioventricular block
If more than two P waves are blocked this is called
advanced second-degree AV block and is often
thought to be pathological, particularly if it does not
disappear with exercise. It has been associated with
disease of the AV node, electrolyte abnormalities and
digitalis toxicity.
EQUINE l CLINICAL HH
Companion Animal Vol 17 June 2012 5
online CPD Third-degree atrioventricular block
A complete dissociation between the atria and
ventricles is referred to as third-degree AV block and
is pathological. There is no electrical conductance
through the AV node and so, in order to contract, the
ventricles must depolarise from an ectopic focus.The
QRS waves generated are therefore of abnormal
morphology and are referred to as escape complexes.
They are not associated with a preceding P wave.
This arrhythmia may be associated with episodes of
collapse if there are insufficient escape complexes to
maintain circulating volume and blood pressure.
Sinus arrhythmia and sinus block
Sinus arrhythmia in the horse is not as common as it
is in small animals. It occurs most commonly on
recovery from exercise. Sinus arrhythmia is
characterised by a regular increase and then decrease
in heart rate and is not considered pathological. It is
thought that this arrhythmia is a result of the switch
from sympathetic to parasympathetic tone following
exercise. Sinus block or sino-atrial block occurs
when the electrical impulse to the heart is blocked
at the sino-atrial node; it is less common than AV
block but is thought to occur due to high vagal tone.
It is not thought to be pathological.
Supraventricular premature
depolarisation (SVPD)
Supraventricular premature depolarisation (SVPDs)
arise from the atria, the AV node or the junctional
tissue. It is more precise to refer to them as SVPDs
Fig. 3: A trace showing a supraventricular premature depolarisation.
EQUINE l CLINICAL HH
Fig. 4: A trace showing atrial fibrillation.
6 Companion Animal Vol 17 June 2012
rather than atrial premature depolarisations, as
differentiation of atrial and junctional origin is
frequently impossible. The PQRS complex occurs
prematurely but a P wave is visible and the QRS is
the same morphology as all the others in the trace
(Fig. 3). The P wave may be of abnormal
morphology, however this is frequently difficult to
detect. Infrequent SVPDs can be seen in normal
healthy horses at rest and at exercise, however
evidence is lacking as to what number may be
considered ‘normal’ (Buhl et al., 2010). It has been
suggested that one per hour is an acceptable normal
limit (Ryan et al., 2005). Numerous SVPDs can be
associated with damage to the atrial myocardium,
atrial enlargement and electrolyte imbalances. Even
though in themselves SVPDs may not cause a
problem, they do predispose to the development of
atrial fibrillation and a detailed cardiac work-up is
required to eliminate cardiac pathology.
Atrial fibrillation (AF)
AF is one of the most common pathological
arrhythmias identified in the horse (Deem et al.,
1982). Large-breed athletic horses are particularly
susceptible, due to the large size of their atria and a
high level of vagal tone. The majority of horses with
AF have no underlying cardiac disease but the
potential for underlying cardiac pathology should
be investigated.
Atrial fibrillation occurs when the atria are
electrically unstable and no longer contract in a
© 2012 Blackwell Publishing Ltd
 coordinated manner. This can be due to myocardial
damage, atrial inhomogeneity or frequent
supraventricular premature depolarisations. The
ECG trace is characterised by an irregularly irregular
rhythm, the heart rate may be normal or elevated,
there are no visible P waves and instead fibrillation
(F) waves are present (Fig. 4). Detailed examination
of the cardiovascular system is required in any horse
diagnosed with AF to ensure the heart is coping. Any
evidence of underlying cardiac pathology will reduce
the likelihood of the horse responding to treatment.
Ventricular premature depolarisations (VPD)
These complexes arise from the ventricles. As a
result, the electrical signal does not follow the
normal pathway and so the resulting QRS complex
is abnormal. They occur early and are not associated
with a P wave (Fig. 5). Like supraventricular
premature depolarisations, occasional VPDs are seen
in normal healthy horses at rest and after exercise,
but the number classified as abnormal is unknown
(Ryan et al., 2005). VPDs should not occur at
exercise in the normal horse and a horse with
frequent VPDs at exercise is not safe to ride because
of the risk of ventricular tachycardia and ventricular
fibrillation. If frequent VPDs occur, their
morphology should be noted: VPDs occurring
frequently, with the same morphology, are referred
to as monomorphic and originate from the same
ectopic focus; those with differing morphologies are
referred to as polymorphic and are likely to arise
from a number of foci. Polymorphic VPDs are of
Fig. 5: A trace showing a ventricular premature depolarisation.
Fig. 6: A trace showing ventricular tachycardia.
© 2012 Blackwell Publishing Ltd
more concern than monomorphic VPDs because
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they imply multifocal ventricular pathology. Further
investigation is required if VPDs are identified.
Ventricular tachycardia (VT)
Ventricular tachycardia is defined as more than four
ventricular premature depolarisations occurring in
sequence. Horses in ventricular tachycardia can often
present with a depressed demeanour and sometimes
even show signs of colic. VT can be caused by
primary disease of the ventricular myocardium,
hypoxia or electrolyte abnormalities. As with VPDs it
is important to establish whether the ventricular
tachycardia is monomorphic or polymorphic. The
R-R interval can be regular, with monomorphic
persistent VT. Horses with ventricular tachycardia
require immediate treatment if they exhibit
polymorphic tachycardia, if their heart rate is above
120 beats per minute, if they have clinical signs of
cardiovascular compromise or if they exhibit an R
on T phenomenon, which indicates significant
instability (Van Loon et al., 2010). Horses with VT are
at risk of going into ventricular fibrillation in which
the ventricles fail to contract in a coordinated fashion.
Ventricular tachycardia is frequently, and rapidly, fatal.
CONCLUSION
Interpretation of the equine electrocardiogram can
be challenging. Even when a diagnosis is reached,
assessing the impact on the horse’s safety to ride is
not straightforward. It is important to become
familiar with the normal ECG so that the best traces
can be obtained, giving the most amount of
information. An understanding of how the
arrhythmias arise helps to assess their significance.
Every arrhythmia detected should be interpreted in
the context of the patient on an individual basis.
REFERENCES
BUHL, R., MELDGAARD, C. and BARBESGAARD, L. (2010) Cardiac
arrhythmias in clinically healthy showjumping horses. Equine
Veterinary Journal 42:196- 201.
DEEM, D. A. and FREGIN, G. F. (1982) Atrial fibrillation in horses: a
review of 106 clinical cases, with consideration of prevalence, clinical
signs and prognosis. Journal of the American Veterinary Medical
Association 180:261-265.
RAEKALLIO, M. (1992): Long-term ECG recording with Holter
EQUINE l CLINICAL HH
Companion Animal Vol 17 June 2012 7
UKVet CeleBRATeS lAUnCH monitoring in clinically healthy horses. Acta Veterinaria Scandinavica

oF neW WeBSiTe
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33:71-75.
RYAN, N., MARR, C. M. and McGLADDERY, A. J. (2005) Survey of
cardiac arrhythmias during submaximal and maximal exercise in
Thoroughbred racehorses. Equine Veterinary Journal 37:265-268.
VAN LOON, G. and PATTESON, M. (2010) Electrophysiology and
arrhythmogenesis. In: Cardiology of the Horse, 2nd Edition. Edited by

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