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How to recognise
common ECG
abnormalities
I
t is important to remember that the primary purpose
of the ECG is to define rhythm disturbances and that
the ECG does not provide information about
myocardial function, whether heart failure is present,
or about the heart valves or endocardium. It is
relatively insensitive to changes in chamber
dimensions and some degree of misinterpretation is
possible if the patients body conformation is not taken
into consideration.
Abnormalities of complex amplitude,
duration or configuration
Unless indicated otherwise, this refers to lead II.
Increased P-wave amplitude (Figure 1)
P-wave amplitude >0.4mV (dog) or >0.2mV (cat).
Usually associated with right atrial enlargement
(due to cor pulmonale or congenital heart disease
such as atrial septal defect or tricuspid valve
dysplasia) or pulmonary disease.
In cats also sometimes seen with hyperthyroidism
and hypertrophic cardiomyopathy.
Increased P-wave amplitude may also be seen at
rapid heart rates.
Sometimes P-wave amplitude increases due to
right atrial enlargement are also accompanied by
an atrial T-wave (a T
A
wave) manifested as a
negative deflection of the baseline in the PR
segment.
Increased P-wave duration (Figure 2)
P-wave duration >0.04 seconds (dog or cat).
Usually associated with left atrial enlargement,
most commonly due to acquired mitral valvular
insufficiency but may also be seen with conduction
abnormalities between SA node and AV node.
Also sometimes seen in congenital defects such as
aortic stenosis, ventricular septal defect (VSD) and
patent ductus arteriosus (PDA).
Jon Wray of Dick White Referrals continues
last months discussion of ECG evaluation by
taking us through common abnormalities
Figure 1: Tall P-waves (0.5 mV) of normal duration in a West
Highland White Terrier with cor pulmonale secondary to
idiopathic pulmonary fibrosis. Note also the deep S-waves.
Lead II, paper speed 25 mm/s, 10 mm = 1 mV
Figure 2: Wide P-waves (and tall T-waves) in a dog with
myxomatous mitral valve disease (MMVD) and marked left
atrial enlargement. P-wave duration is approximately 0.06
seconds and a notched appearance is noted. The tall T-waves
in this patient were not due to hyperkalaemia but may have
been due to an increased left ventricular repolarisation
vector or possibly myocardial hypoxia. Lead II, paper speed
50 mm/s, 10 mm = 1 mV
Increased P-wave amplitude and duration
Usually indicates bi-atrial enlargement.
Increased R-wave amplitude (Figure 3)
Great care must be taken to interpret R-wave
amplitude in conjunction with the conformation of the
patient, bearing in mind that the principal determinants
of potential difference measured are not only the size
of the potential difference generated by cardiac tissue
but also the effects of electrical impedence caused by
the distance between recording electrodes and the
cardiac surface and the amount of body fat present
(as well as any fluid e.g. pleural or pericardial
effusions).
R-wave amplitude >2.5mV or >3mV in
thin-chested breeds (dogs) or >0.9mV (cats).
Usually indicative of left ventricular enlargement
and often accompanied by prolonged QRS
duration.
Usually associated with eccentric hypertrophy due
to left ventricular volume overload due to acquired
mitral valve disease, primary myocardial disease
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such as dilated cardiomyopathy or congenital heart
defects leading to left ventricular volume overload
(e.g. PDA, VSD) or concentric hypertrophy due to
pressure overload (e.g. aortic stenosis).
Decreased R-wave amplitude
The lower limit for R-wave amplitude is highly
variable in cats and dogs, without strict limits; to a
certain degree experience with normal ECGs from
various breeds (especially of dogs) is helpful in
determining whether R-wave amplitude is lower
than expected. Arbitrarily R-wave amplitude
<0.5mV in all of leads I,II and III in dogs is often
taken as indicative of low R-wave amplitude. Dogs
with giant, barrel-shaped conformation (such as
StBernards) may normally have a surprisingly
small R-wave amplitude due to the degree of
electrical impedence present.
Pathological conditions resulting in decreased
R-wave amplitude include pleural and pericardial
effusions.
Electrical alternans
Variation in R-wave amplitude increasing and
decreasing in a cyclical fashion may be seen in
animals with pericardial effusion and is considered
Figure 4: Increased QRS complex duration (0.08 seconds) due
to left ventricular enlargement in a Dobermann with dilated
cardiomyopathy. P-waves are also wider than normal,
suggesting that left atrial enlargement is also present, and
the R-wave slurs into the T-wave, a feature commonly seen
with left ventricular enlargement. Lead II, paper speed
50 mm/s, 10 mm = 1 mV
Figure 3: (A) Increased R-wave amplitude (2.3 mV) in a cat
with severe left ventricular hypertrophy due to hypertrophic
cardiomyopathy. Lead II, paper speed 25 mm/s, 10 mm =
1 mV. (B) Increased R-wave amplitude (3.5 mV) in a dog with
left ventricular volume overload due to patent ductus
arteriosus. Lead II, paper speed 25 mm/s, 10 mm = 1 mV.
In this case the dog was a young adult of normal body
condition/conformation; in many puppies with PDA
increased R-wave amplitude may also be due to lack of
electrical impedence caused by small body size/lack of fat
A
B
to be due to alteration in the principal
depolarisation vector as the heart swings back
and forth within a fluid-filled pericardial sac.
Increased QRS duration (Figures 4 and 5)
QRS duration >0.05 s (>0.06 s giant breeds)
(dogs), >0.04 s (cats).
Increased QRS duration signifies prolonged
depolarisation of ventricular muscle tissue or a
conduction disturbance, or both. This may result
from three circumstances:
The origin of the depolarising stimulus is a
normal sinus beat but EITHER
An increased ventricular (principally left
ventricular) muscle mass is depolarised
e.g. with left ventricular hypertrophy
(Figure4) OR
The sinus beat is conducted abnormally
(slowly) upon reaching the ventricular
conducting system by an intraventricular
conduction defect such as in the case of a
bundle branch block (Figure 5).
The complex is an ectopic one, arising from
outside the specialized conduction system of
the heart and below the level of the AV node.
Therefore, when increased QRS duration is
recognised it is important to evaluate whether a
P-wave is associated with the QRS complex (i.e. if
there is a P-wave for every QRS and a QRS for
every P the diagnosis is most likely a sinus beat
conducted with a block or increased left ventricular
muscle mass).
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How to recognise
common ECG abnormalities
S1, S2, S3 pattern (Figure 6)
In the dog S-waves are usually only seen in lead III
but may sometimes be seen in lead II. Presence of
an S-wave in leads I, II and III, however, is usually
indicative of right ventricular enlargement. Note
that this can be a normal finding in cats.
variations are quite normal. In general T-waves
should be <25% the R-wave amplitude but this
does not hold true at low R-wave amplitudes.
T-waves may be normally positive, negative or
biphasic in lead II in dogs and cats.
Tall, spiky T-waves (Figure 7) which are >25% the
R-wave amplitude are classically seen in patients
with hyperkalaemia, though caution should be
exercised in trying to draw clinical parallels
between T-wave morphology and severity of
hyperkalaemia as is implied in some textbooks. In
the authors experience severe hyperkalaemia may
exist in the absence of T-wave abnormalities, and
abnormalities are frequently inconsistent in their
magnitude in the same individual at different
severities of hyperkalaemia.
Figure 5: In this dog a normal sinus origin beat is conducted
with a right bundle branch block (BBB) resulting in a wide
and bizarre QRS complex, even though the rhythm is
supraventricular. Lead II, paper speed
25 mm/s, 10 mm = 1 mV
Figure 7: Tall, spiky T-waves in a canine patient with
hyperkalaemia of 7.4 mmol/l due to hypoadrenocorticism.
Lead II, paper speed 25 mm/s, 10 mm = 1 mV. Such
abnormalities are, however, inconsistent in hyperkalaemic
patients and severity of ECG changes does not necessarily
mirror severity of hyperkalaemia
Figure 6: S1, S2, S3 pattern in a Miniature Schnauzer with
pulmonic stenosis. Leads I, II, III, paper speed 25 mm/s,
10 mm = 1 mV
Deep Q-waves in I, II, III and aVF
In smaller breeds of dog may signify right
ventricular enlargement but can be a normal
finding in large breeds and in cats.
QRS splintering
Splintered QRS complexes are notched in a way
that produces at least 2 R-waves in a Rr, RR, rR
or rr configuration and are most commonly seen in
dogs with tricuspid valve abnormalities, especially
in Labrador Retrievers with tricuspid valve
dysplasia.
T-wave
The T-wave represents ventricular repolarisation.
There are very few restrictions of interpretation on
T-wave morphology and size, since many
Abnormalities of inter-complex segments
PR interval
The PR interval comprises the P-wave and the PR
segment and represents the period from initiation
of atrial depolarisation to the initiation of ventricular
depolarisation. The majority of this time interval, the
PR segment, is due to the slowed conduction
through the atrioventricular (AV) node (which
occurs at 0.050.1m/s in the upper part of the AV
node compared with 0.51m/s in atrial
myocardium and 24m/s in the Purkinje network).
PR interval prolongation >0.13s (dogs) or >0.09s
(cats) represents first-degree AV block (Figure 8).
This may occur with increased vagal tone, atrial
myocardial or AV nodal disease, hyperkalaemia,
endotoxaemia and drug therapy (digitalis
glycosides, calcium channel blockers, beta
blockers and class I anti-arrhythmics).
ST segment
The ST segment is a time of early repolarisation but
should be isoelectric in healthy animals.
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Slurring of the ST segment such that the end of
the S-wave slews into the T-wave without return to
a steady baseline is usually indicative of left
ventricular enlargement.
ST segment elevation (>0.15mV) or depression
(>0.2mV) (Figure 9), when compared with the
pre-P-wave baseline, is frequently taken to be
indicative of myocardial hypoxia or ischaemia,
though it may also be seen with myocarditis,
pericarditis, hypertrophy and calcium abnormalities.
Caution must be applied in avoiding
overinterpretation of QT intervals in dogs and cats
as much normal variation is seen.
Prolonged QT intervals may be seen in
hypocalcaemia, hypokalaemia, hypothermia,
ethylene glycol toxicity and in the presence of
intraventricular conduction defects.
Shortened QT intervals may be seen in
hypercalcaemia, hyperkalaemia and in digoxin
toxicity.
Abnormalities of relationship between
P-waves and QRS complexes
P-waves are present without associated
QRS complexes
The presence of non-conducted P-waves usually
indicates second-degree or higher atrioventricular
block. It may occasionally be seen in non-
conducted atrial premature complexes (see below)
which arise whilst the AV node is still in its
refractory period.
Second-degree AV block
Second-degree AV block is characterised by
intermittent failure of AV conduction (by definition if
constant failure were to occur atrial and ventricular
depolarisation would occur at independent rates
and complete AV block would be occurring) and
may be classified as Mobitz type I (Wenckebach
phenomenon) or Mobitz type II, but confusingly
may also be described as Type A (normal QRS
duration)/Type B (prolonged QRS duration) and
low-grade/high-grade (high grade usually being
defined as any block of 2:1 relationship or greater)
Mobitz Type I (Wenckebach) second-degree
AV block is characterised by a regularly
irregular rhythm in which the RR interval
shortens and the PR interval prolongs until a
blocked P-wave occurs. The heart rate may be
slow but is often normal. Both the P-wave and
QRS complex are usually normal in duration
and morphology.
Mobitz Type II second-degree AV block
(Figure 10) is characterised by a constant PR
interval when P-waves are conducted in a fixed
relationship between atrial and ventricular
conduction (e.g. 2:1, 3:1, 4:1). Bradycardia
normally exists. QRS morphology is often
abnormal, indicating the involvement of the
bundle of His or proximal bundle branches.
Figure 8: First-degree AV block
with PR interval of 0.36
seconds in a canine patient
with no evidence of structural
or functional cardiac disease
but with severe
gastrointestinal signs. Lead II,
paper speed 50 mm/s, 10 mm
= 1 mV
Figure 9: Marked ST segment depression of 0.3 mV in a
Greyhound which had suffered prolonged seizure activity
and suspected consequent myocardial hypoxia. Atrial
standstill is also present. Leads I and II, paper speed
50 mm/s, 10 mm = 1 mV
QT interval
The QT interval represents the time taken for
complete ventricular depolarisation then
repolarisation (i.e. the whole of electrical systole)
and will vary inversely with heart rate, shortening at
higher rates.
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Low grade and type I second-degree AV block
may be associated with elevated vagal tone
(especially due to gastrointestinal or respiratory
disease); reassessment of an ECG after
administration of a vagolytic such as atropine may
be used to confirm this.
Higher grade/type II second-degree AV block is
usually associated with degenerative or
inflammatory processes involving the AV nodal
conduction tissue, and a form of hereditary AV
nodal stenosis is seen in Pugs. Digoxin toxicity
may cause a variety of AV nodal conduction
abnormalities. High grade/type II second-degree
AV block often is progressive and leads to
symptomatic bradydysrhythmias necessitating
pacemaker implantation. The prognosis with type I
second-degree AV block is generally more
favourable.
Third-degree AV block is described below under
There is no relationship between P-waves and QRS
complexes.
QRS complexes are present without
associated P-waves
The presence of QRS complexes without
preceding P-waves usually indicates one of:
Atrial fibrillation
Atrial standstill
Ventricular premature or escape complexes
AV nodal premature or escape complexes
Ventricular tachycardia.
Atrial flutter may have P-waves that are visible
more as a saw-toothed baseline and so may be
seen without typical associated P-waves, though
they are present.
Assessment of the QRS complex morphology,
especially in determining are the complexes tall
and narrow or wide and bizarre?, is useful in
differentiating between these. Tall and narrow
complexes are always supraventricular in origin.
Wide and bizarre complexes are usually ventricular
in origin but some circumspection must be applied
since supraventricular complexes accompanied by
an interventricular conduction disturbance such as
a bundle branch block may appear wide. This is
easily identified if P-waves are present and their
relationship with the QRS obvious but in some
tachydysrhythmias in particular the P-waves may
be hidden in the preceding QRST arrangement
and difficult to isolate.
There is no relationship between P-waves
and QRS complexes
Most commonly this occurs when there are
separate pacemakers controlling atria and
ventricles and/or where there is complete
(third-degree) AV block. The term atrioventricular
dissociation has often unfortunately been used
synonymously with third-degree AV block but
whilst third-degree AV block is a form of
atrioventricular dissociation it is not the only one.
Third-degree AV block (Figure 11)
In third-degree AV block there is no conduction
between the atria and ventricles and whilst the
sinus node depolarises at its own inherent rate,
producing P-waves, the ventricles depolarise in
a fashion and rate dictated by a subsidiary
(failsafe) pacemaker, usually in the AV node or
Purkinje fibres.
There is no relationship between P-waves and
QRS complexes and the PR interval is
variable.
Third-degree AV block is usually considered a
degenerative/destructive condition of the AV
conduction fibres, though occasional cases
may be associated with inflammatory disorders
(myocarditis) and very occasionally apparent
spontaneous resolution may be seen.
Isorhythmic AV dissociation (Figure 12)
This is an unusual arrhythmia, sometimes
termed accrochage or synchronisation, in
How to recognise
common ECG abnormalities
Figure 11: Third-degree AV block in a canine patient.
Ventricular depolarisation rate is of 36/min, atrial
depolarisation rate is of 176/min. Lead II, paper speed
50 mm/s, 5 mm = 1 mV
Figure 10: Both first-degree (PR interval 0.16 seconds) and
Mobitz type II second-degree AV block are present in this
canine patient with aortic stenosis and secondary left
ventricular concentric hypertrophy. Lead II, paper speed
50 mm/s, 5 mm = 1 mV
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which atria and ventricles are depolarised by
separate and electrically discontinuous
pacemakers at rates which approximate one
another, but where no precise relationship
exists between atrial and ventricular
depolarisations.
This usually occurs when a ventricular, or more
usually an AV nodal ectopic, pacemaker is
depolarising at a rate which is slightly faster
that the sinus node rate
We see this most commonly in feline patients
under anaesthesia, both with and without
echocardiographically identifiable structural
heart disease, and in these cats the rhythm
usually resolves with attainment of normal sinus
rates upon cessation of anaesthesia.
Isorhythmic AV dissociation is characterised by
P-wave and QRS complex rates which
approximate one another but are not precisely
the same; whilst the PP and the RR intervals
are constant, the PR interval varies slightly
with the result that the P-waves appear to
march in-and-out of the QRS complexes.
Supraventricular rhythm disturbances
Sinus arrhythmia
Although this is a physiologically normal
phenomenon its irregularity classifies it as an
arrhythmia as, whilst the rhythm originates from the
sinus node, the rhythm is regularly irregular. This
raises an important issue, that sinus arrhythmia will
only be recognised as such (i.e. an important
normal physiological finding) if (a) the patient is
auscultated or an ECG performed for long enough
for a pattern to be established and (b) the
examiner interprets the heart rhythm in concert
with the respiratory pattern.
Sinus arrhythmia is a normal finding in dogs but is
unusual in cats without respiratory disease. It may
be particularly exaggerated in brachycephalic
breeds and in those with enhanced vagal tone due
to respiratory or gastrointestinal disease.
During inspiration the heart rate accelerates and
decelerates or pauses during expiration due to
fluctuations in vagal tone. It may also be
associated with a wandering sinus pacemaker, in
which P-wave amplitude varies cyclically, usually
becoming peaked during inspiration and flatter
during expiration. Occasionally non-respiratory
sinus arrhythmia may be encountered in which
there is no relationship with respiration.
Sinus bradycardia
Sinus bradycardia is a rhythm originating from the
sinus node at <60 beats/min (dogs) and <100
beats/min (cats). However, care should be taken to
interpret it in the light of the animals level of fitness
(especially in dogs).
Common causes include hypothermia, increases in
vagal tone (especially due to respiratory and
gastrointestinal disease), neurological lesions
(especially of the brainstem, and in tonsillar
herniation and raised intracranial pressure), severe
systemic metabolic conditions, preceding cardiac
arrest, sinus node dysfunction (such as sick sinus
syndrome) and drug intoxication (especially
opiates, digoxin, calcium channel and beta
blockers). It should be remembered that in many
cats shock results in bradycardia rather than
tachycardia.
On the ECG the P-wave morphology and
measurements, QRS morphology and
measurements, timing intervals between
complexes and association are all normal, but the
rate is slow.
Sinus arrest (Figure 13)
Sinus arrest is caused by failure of impulse
formation within the sinoatrial node. Sinus arrest
occurs when there is a pause in sinus node activity
Figure 12: Isorhythmic AV dissociation in a 10-year-old
Domestic Shorthair cat under general anaesthesia for an
orthopaedic surgical procedure. The ventricular
depolarisation rate is approximately 115/min and the atrial
depolarisation rate is approximately 107/min when
instantaneous rates are calculated. No structural heart
disease was found to be present and a normal sinus rhythm
with rate of 168/min was recorded after recovery from
anaesthesia. Leads I,II,III, paper speed 25 mm/s, 20 mm =
1 mV
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for more than two normal RR intervals, though
there may be some overlap with exaggerated sinus
arrhythmia, where pronounced pauses may also
be seen.
In dogs this is usually due to either sinus node
dysfunction (e.g. in sick sinus syndrome), severe
disease of the atria, severe hyperkalaemia or
digoxin intoxication or as a result of increased
vagal tone, and administration of a vagolytic such
as atropine may be used to determine the latter.
A period of sinus arrest is often terminated by an
escape beat which may be either nodal or
ventricular.
Sinus (sinoatrial) block (Figure 14)
Sinoatrial block occurs where the sinoatrial node
depolarises normally but fails to conduct through
tissue surrounding the node, therefore failing to
depolarise the atria.
Although sinoatrial block and sinus arrest may be
difficult to distinguish, when the length of pause
before a subsequent beat is an exact multiple of a
normal RR interval a sinoatrial block is strongly
implicated.
Sinoatrial block is usually caused also by sinus
node dysfunction, severe disease of the atria or
increased vagal tone.
Persistent atrial standstill (Figure 15)
In persistent atrial standstill the sinoatrial node is
inactive and the rhythm is a regular
supraventricular escape rhythm characterised by
lack of P-waves and by regular QRS complexes
which are tall and narrow in morphology.
Persistent atrial standstill has been recognised
most commonly in English Springer Spaniels
and in dogs with severe muscular heart disease
or generalised muscular dystrophies but is
also seen in severe hyperkalaemia and in
digoxintoxicity.
How to recognise
common ECG abnormalities
Figure 13: A period of sinus arrest lasting approximately 6.5
seconds in a 7-year-old female entire Irish Terrier. After the
period of arrest a supraventricular escape beat occurs from a
site outside the SA node in which the P-wave occurs
between the QRS complex and the T-wave. Leads I, II, III,
paper speed 25 mm/s, 5 mm = 1 mV
Figure 14: Sinus block in a canine patient. Lead II, paper
speed 50 mm/s, 10 mm = 1 mV. Note that the RR-2 interval
(48 small squares) is an exact multiple, x2, of the RR-1
interval (24 small squares)
Figure 15: Lead II LED display from a continuous monitor of a
5-year-old Springer Spaniel with collapse due to persistent
atrial standstill. A regular, wide-complex escape rhythm of
50/min is present
Atrial premature complexes (atrial
premature depolarisations)
APCs arise from an ectopic focus within the atria
and are characterised by:
A shortened RR interval
A P-wave which is premature (P) which
disrupts the normal rhythm. The P-wave is
often different in morphology from the normal
P-waves and may be positive negative or
biphasic
Normal QRS complex morphology and
duration
If a P-wave occurs early enough that the AV
node is still in its refractory period it may be
non-conducted.
Atrial premature complexes, if occurring in
isolation, are usually unassociated with clinical
signs though they may indicate atrial enlargement,
atrial disease, drug therapy or be associated with
systemic conditions.
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Supraventricular escape rhythms
Escape complexes follow an RR interval that is
longer than the normal RR interval and occur at
an (instantaneous) heart rate that is equivalent to
the intrinsic rate of the pacemaker from which the
escape complex originates. In the case of
supraventricular escape beats, this is usually the
AV node and is known as a junctional escape. This
rate is usually 4060 beats/min, though may be
faster (enhanced).
Atrial fibrillation (Figure 16) and atrial
flutter
Atrial fibrillation is characterised by absence of
P-waves, by QRS complexes which are usually tall
and narrow (though occasionally may be wide and
bizarre if a concurrent conduction disturbance
such as bundle branch block is seen) and by a
completely irregular RR interval. The baseline
may contain large oscillations (F-waves) though
more commonly these are small and appear as a
more shuddering baseline.
Most commonly atrial fibrillation occurs with high
QRS rates of 180240/min (dogs) or 200260/min
(cats) and usually accompanies severe structural
heart disease (Figure 16A). However, in some
patients (usually dogs without heart failure) lower
ventricular depolarisation rates are seen, in the
120180/min range, due to fewer fibrillating
potentials reaching the ventricles. The lower rate in
these patients is because they have higher vagal
tone compared with patients in heart failure and
this influences the refractory period of the AV node.
Presence of atrial fibrillation without underlying
identifiable cardiac morphological changes is often
termed lone or primary AF and is most often
seen in giant breed dogs (Figure 16B). In cats
atrial fibrillation is uncommon and is almost always
associated with structural cardiac disease.
Atrial flutter is rare and is a very fast
supraventricular tachycardia in which atrial
depolarisation rates are so high that the PP cycle
length is short enough that atrial depolarisation
reaches the AV node whilst the latter is still in its
refractory period. This results in functional
second-degree AV block P-waves are non-
conducted because they reach the AV node during
this refractory period. ECG characteristics of atrial
flutter are irregular RR intervals and a rapid
saw-toothed baseline to the ECG, representing
very rapid, only intermittently conducted, P-waves
at rates which usually exceed 350400 beats/min
in the dog.
Supraventricular tachycardia (Figure 17)
A full discussion of supraventricular
tachydysrhythmias is beyond the scope of this
article but supraventricular tachycardia is
characterised by recurrent supraventricular
premature depolarisations.
These may occur within the atria or nodal tissue
and most commonly have a normal (tall and
narrow) QRS morphology, though confusion with
ventricular tachycardias may arise in those patients
with co-existing bundle branch block.
P-waves may or may not be present, depending on
the site of origin of the supraventricular tachycardia.
Figure 16: (A) Atrial fibrillation in an Irish Wolfhound with
dilated cardiomyopathy (DCM). The ventricular rate is 200/
min. Note the fine fibrillation potentials (F-waves) of the
baseline, no discernible P-waves and completely irregular RR
intervals. Lead II, paper speed 25 mm/s, 10 mm = 1 mV.
(B) Primary or lone atrial fibrillation in a giant breed dog
without evidence of structural heart disease or clinical signs
of heart failure. The ventricular rate was 156/min. Lead II,
paper speed 50 mm/s, 10 mm = 1 mV
A
B
Figure 17: Supraventricular tachycardia of approximately 300
beats/min. Note the tall and narrow QRS complexes. In this
example the P-waves are frequently seen between the QRS
complex and T-wave of the preceding beat. Lead II, paper
speed 25 mm/s, 10 mm = 1 mV
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How to recognise
common ECG abnormalities
Supraventricular tachycardia usually occur
secondary to organic heart disease and, broadly,
may be caused by re-entrant circuits as a result of
diseased tissue, presence of an accessory
conduction pathway or may be initiated by
abnormal automaticity of supraventricular tissues.
It is very important, before embarking on any
therapeutic decisions relating to documented
tachycardias, to establish that the rhythm is not in
fact a sinus tachycardia which may be
physiologically appropriate (in fearful, stressed or
painful patients), a normal adaptation to a systemic
disease state (e.g. fever, anaemia) or a life-
preserving response (e.g. in compensatory shock
states), as inappropriate interpretation and
anti-arrhythmic treatment may at best be
unnecessary and at worst cause acute
decompensation of the patient.
Ventricular rhythm disturbances
Ventricular rhythm disturbances are characterised by
wide and bizarre QRS complexes though some
caution should be exercised, as supraventricular
originating complexes that are conducted abnormally
(for instance with bundle branch block) may also have
wide and bizarre morphology.
Ventricular escape complexes and
idioventricular rhythm
Escape complexes (Figure 18) follow an RR
interval that is longer than the normal RR interval
and occur at an (instantaneous) heart rate that is
equivalent to the intrinsic rate of the pacemaker
from which the escape complex originates. In the
case of ventricular escape beats, this is usually
the Purkinje apparatus and the rate is usually
2040 beats/min. In the case of junctional
escapebeats this is usually at a rate of 4060
beats per minute.
When both sinoatrial node depolarisation fails and
the next highest-rate subsidiary pacemaker (the
junctional tissue) also fails, the ventricles may be
depolarised at a rate consistent with the intrinsic
rate of the Purkinje apparatus, producing an
idioventricular rhythm. We recognise this most
commonly in severe disease states causing atrial
standstill, such as in hyperkalaemia produced by
hypoadrenocorticism or urinary tract obstruction.
Itis important to recognise idioventricular rhythm
as a life-saving failsafe and to promptly correct the
underlying cause. Suppression of the rhythm with
anti-arrhythmics may be fatal.
Ventricular premature complexes
(ventricular premature depolarisations)
VPCs are characterised by a wide and bizarre QRS
complex with a T-wave which is opposite in polarity,
occurring without a P-wave and after an RR
interval that is shorter than the normal RR interval.
VPCs usually originate from the right ventricular
tissue if they are predominantly positive in leads I,
II, III and aVF and from the left if they are
predominantly negative in these leads.
VPCs may be seen in normal animals at a rate of
up to 50 per 24 hours but most commonly in
veterinary patients are associated either with
structural cardiac disease or with systemic
diseasestates and intoxications. It is useful to
consider the mnemonic think AHEAD! when it
comes to recalling non-cardiac causes of
ventricular rhythm disturbances:
Autonomic neurological disturbances
Hypoxaemia
Electrolyte and acidbase disturbances
Abdominal diseases, especially of the spleen,
stomach and pancreas
Drugs and intoxicants, especially in the
peri-anaesthetic period.
Presence of ventricular premature complexes,
however isolated, attains a greater level of
significance in those breeds in which
arrhythmogenic sudden death due to occult
cardiac disease is well documented (the
Dobermann and the Boxer) and when VPCs are
multiform in nature.
Ventricular tachycardia (Figures 19 and 20)
Ventricular tachycardia is defined as three or more
consecutive ventricular premature complexes.
The rate at which a ventricular tachycardia is
determined is not well established but it is often
considered a tachycardia at rates exceeding
180bpm and an accelerated idioventricular rhythm
(see below) at rates below this.
Figure 18: A wide and bizarre QRS complex without
preceding P-wave occurs in this patient after a period of
sinus arrest. This complex is a ventricular escape. Lead II,
paper speed 25 mm/s, 5 mm = 1 mV
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Like VPCs (above) ventricular tachycardia may be
caused by cardiac and non-cardiac causes and
consideration of the components of the think
AHEAD menemonic is always recommended in
patient evaluation.
The degree of malignancy or perspicuity required
in treatment of ventricular tachycardias is often
based on consideration of:
Absence of AHEAD criteria as defined above
Association with clinical signs of reduced
cardiac output (syncope, collapse, poor
peripheral pulse quality, hypotension), which
tends to be determined by the absolute rate of
the tachycardia and thus the time available for
diastolic ventricular filling and subsequent
output
Occurrence in a breed, such as a Dobermann
or Boxer, with a known risk of arrhythmogenic
sudden death
Morphology of the ventricular premature
complexes being:
Multiform rather than monomorphic
Having R-on-T phenomenon the
absence of a baseline interval between the
T-wave of the preceding QRST wave with
start of the QRST of the next, resulting in
the R-wave being continuous with the
preceding T-wave (see Figure 19).
Accelerated idioventricular rhythm
Defined as a constant ventricular origin rhythm that
is above the rate expected for an idioventricular
rhythm (see above) but below the level at which
ventricular tachycardia is recognised.
Most dogs with accelerated idioventricular rhythm
have rates between 150 and 180/min and a regular
wide and bizarre QRST complex with no visible
P-waves.
The rhythm is usually not highly haemodynamically
significant, as the ventricular rate is such that
adequate diastolic filling can occur, and it is rare
that such rhythms are associated with any
decrease in cardiac output.
Accelerated idioventricular rhythms are most
commonly seen in the first 2448 hours after
surgery for splenic pathology (especially
ruptured splenic mass lesions) and for gastric
dilatationvolvulus.
Whilst it is tempting to give anti-arrhythmic
therapy, in the majority of cases this is not
required and the rhythm will resolve with time
and with provision of adequate fluid support,
attention to correction of arrhythmia-
potentiating electrolyte disturbances
(particularly hypokalaemia and
hypomagnesaemia) and analgesia.
The author recommends caution in these
circumstances as it is his experience that
such a rhythm disturbance often distracts
the veterinary care team, causing
concentration on the ECG in isolation from
the rest of the patient, rather than interpretation
in the context of historical, medical and,
most importantly, physical examination
findings!
Conclusion
Provided that a logical and systematic approach is
used to both obtain a diagnostic ECG and to interpret
it in a stepwise manner, most common ECG
abnormalities can be readily identified. In particular,
evaluating critically the relationship between the
P-and QRS-waves and taking the time to measure
and record findings, rather than to merely eyeball an
ECG, will result in more accurate diagnosis and less
reliance on pattern recognition.
Figure 20: Ventricular tachycardia in a 5-year-old MN Sphynx
cat presenting with syncope. The complexes are wide and
bizarre, without preceding P-waves, and the rate of the
ventricular tachycardia is about 272/min. A single normal
sinus complex is seen in the centre of the trace (complex 9).
Lead II, paper speed 50 mm/s, 10 mm = 1 mV
Figure 19: Frequent non-sustained ventricular tachycardia.
In this patient there are several criteria which would suggest
that this rhythm is malignant and that sudden death is a
risk, including the multiform nature of the ventricular
premature depolarisations and the frequent occurrence of
R on T phenomenon (within black ovals). Leads I, II, III,
paper speed 25 mm/s, 10 mm = 1 mV
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