ECG interpretation in small animals

December 14, 2017 | Author: gacf1974 | Category: Cardiac Arrhythmia, Electrocardiography, Heart, Atrium (Heart), Heart Rate
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A good understanding of the electrical activity of the heart is key to the accurate interpretation of ECGs

ECG interpretation in sm~all anim~als 1. Understanding the electricity of the heart MIKE MARTIN THIS article, the first of three aimed at assisting those in practice in interpreting electrocardiograms (ECGs), discusses the electrical activity of the heart and how this relates to the complexes seen on an ECG. It also describes the clinical findings on auscultation and palpation of the pulse. It must be remembered that an ECG trace should always be interpreted in the light of a thorough clinical examination of the cardiovascular system, with particular attention being paid to heart rate and rhythm, pulse rate, and identification of pulse deficits, if present. The second article in the series, to be published in the next issue, will discuss the abnormalities associated with the conduction system of the heart. The final article, to be published in the May issue, will outline a practical approach to interpreting ECGs. Mike Martin graduated from Dublin in 1986. In 1997, he founded his own cardiorespiratory referral practice, the Veterinary Cardiorespiratory Centre, in Kenilworth, Warwickshire. He holds the certificate and diploma in veterinary cardiology and is an RCVS Specialist in Cardiology. He is the current chairman of the Veterinary Cardiorespiratory Society and is a past recipient of the BSAVA's Dunkin and Melton Awards.

THE ELECTRICITY OF THE HEART

The heart must contract in a coordinated atrioventricular sequence to act efficiently as a 'circulatory pump'. To do this, the cardiac muscle cells must receive an electrical stimulus. It is this electrical activity that is detected by an electrocardiograph (see box below). The electrical stimulus must first depolarise the two atria and then, with an appropriate time interval, stimulate the two ventricles. The heart must then repolarise (while 'refilling') in time for the next electrical stimulus and contraction and must do so repeatedly, increasing in rate with a rise in demand and, conversely, slowing at rest.

Atrioventricular node

\

Atrioventricular

/Sinoatrial node

\ring|

Left atrium

Right atrium | \ | \\

Bundle of His

J

~~~~~Left

/ {_ _ ~~~bundle bac

Anterior fascicle

Right bundle branch

Posterior - fascicle

-

Purkinje - fibres

anI Simply put, an electrocardiograph (ECG machine) is a voltmeter (or galvanometer) that records the changing electrical activity of the heart between a positive and negative electrode. Electrocardiography is the process of recording these electrical changes. Although a positive and negative electrode can be placed almost anywe on, or 1n, the body to record electrical changes, the most common and simplest method is to place these electrodes on the legs of an animal. This is referred to as body surface limb ECG recording. 14

The heart's electrical circuit. Reproduced with permission from Blackwell Science

FORMATION OF THE NORMAL P-QRS-T COMPLEX Most of the cells within the heart have the ability to generate their own electrical activity, but the sinoatrial node is the fastest to do so and is, therefore, the 'rate controller' or pacemaker of the heart. The rate of the sinoatrial node is influenced by the balance in autonomic tone, involving the sympathetic (which increases the rate) and parasympathetic (which decreases the rate) systems. The sinoatrial node normally initiates the electrical discharge for each cardiac cycle. Depolarisation spreads In Practice * MARCH 2002

Atrioventricular node I

Sinoatrial_ nodeI

Right

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Partial depolarisation of the atria and formation of the P wave. The shaded area represents depolarised myocardial cells and the arrows show the direction in which the depolarisation wave is travelling. Reproduced with permission from Blackwell Science

through the atrial muscle cells. The depolarisation wave then spreads through the atrioventricular node, but it does so more slowly, thereby creating a time delay. Conduction passes through the atrioventricular ring (from the atria into the ventricles) through a narrow pathway called the bundle of His. This then divides in the ventricular septum into left and right bundle branches (going to the left and right ventricles). The left bundle branch divides further into anterior and posterior fascicles. The conduction tissue spreads into the myocardium as very fine branches called Purkinje fibres. Formation of the P wave From the sinoatrial node, the depolarisation wave spreads through the atria (somewhat like the ripples created by dropping a stone into water). As the first portion of the atria (nearest the sinoatrial node) is depolarised, this creates an electrical potential difference between the depolarised atria and the parts not yet depolarised (ie, those still in a resting state). When negative and positive electrodes are placed in alignment with the right atrium and the left ventricle, respectively, this results in the voltmeter (ie, the ECG machine) detecting the depolarisation wave travelling across the atria in the general direction of the positive electrode. When a depolarisation wave travels towards a positive electrode, this is reflected as a positive (upward) depolarisation on the ECG recording. The atrial depolarisation wave, therefore, creates an upward excursion of the stylus on the ECG paper. When the whole of the atria becomes depolarised, there is no longer an electrical potential difference and so the stylus returns to its idle position (ie, the baseline). The brief upward deflection of the stylus on the ECG paper creates the P wave, representing atrial electrical activity. The muscle mass of the atria is fairly small and so the electrical changes associated with its depolarisation are also small.

InPractice

*

MARCH 2002

Complete depolarisation of the atria and formation of the P wave. Reproduced with permission from Blackwell Science

Formation of the P-R interval The speed with which the electrical depolarisation wave travels through the atrioventricular node is relatively slow so that the ventricular contraction will be timed to occur following atrial contraction and maximal ventricular filling. Once the depolarisation wave passes through the atrioventricular node, it travels very rapidly through the specialised conduction tissues of the ventricles (ie, the bundle of His, the left and right bundle branches and Purkinje fibres).

Formation of the QRS complex It is often quite useful to think of the QRS complex as a whole, rather than in terms of its individual components. The depolarisation wave passes through the atrioventricular node to the rapid conduction tissue of the ventricles. When the ventricular myocardium is depolarised, this creates a depolarisation wave that travels towards the positive electrode; because the ventricular myocardium is a large mass of muscle tissue, this usually creates a large deflection. Hence, the QRS complex is usually large and positive (in lead II).

Depolarisation of the ventricular

the bulk of

myocardium

and formation of the QRS

-------------------complex.

Reproduced with permission from Blackwell Science

115

This is because repolarisation of the myocardium in small animals is a little random compared with humans, for example, in which repolarisation is very organised and the T waves always share the same polarity as the QRS complexes (irrespective of the lead in which the recording is made). The diagnostic value of abnormalities in the T wave of small animals is therefore very limited (whereas abnormal T waveforms in humans can be very useful diagnostic features).

SINUS RHYTHMS A normally formed complex is termed a sinus complex; that is, there is a P wave for every QRS complex and T wave (or vice versa). A sequence of beats originating from the sinoatrial node forms a rhythm, known as the sinus rhythm. There are four common sinus rhythms and these are described below.

Complete depolarisation and repolarisation of the atria and ventricles and completion of the P-QRS-T complex. Reproduced with permission from Blackwell Science

Normal sinus rhythm In normnal sinus rhythm, the stimulus originates regularly at a constant rate from the sinoatrial node (dominant pacemaker), depolarising the atria and ventricles normnally and producing a coordinated atrioventricular contraction. CLINICAL FINDINGS

Formation of the T wave

After complete depolarisation of the ventricles, they then repolarise in time for the next stimulus. This phase of repolarisation creates a potential difference across the ventricular myocardium until it is completely repolarised. This results in a deflection from the baseline (in lead II) which is termed the T wave. The T wave in dogs and cats is very variable and can be negative, positive or even biphasic (ie, a bit of both).

Regular heart sounds are heard on auscultation (ie, lubb dupp) with a pulse for each heartbeat and at a rate which is normal for age, breed and species. ECG FEATURES

The ECG shows a normal P wave followed by normal QRS and T waves. The rhythm is regular (constant) and the rate is normal for age, breed and species. The size of the ECG complexes are typically small in cats and,

QRS

ECG from a dog showing normal sinus rhythm at a rate of 140/minute. (Lead 11, I cm/mV, 25 mm/second)

~

ECG from a cat showing normal sinus rhythm at a rate of 220/minute. Some baseline drift associated with movement during the ECG recording can also be seen. (Lead 11, I cm/mV, 25 mm/second)

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ECG from a dog showing

respiratory sinus arrhythmia at a rate of approximately 100/minute. Note also the slight variation in P wave amplitude - this is termed

wandering pacemaker. (Lead 11, I cm/mV, 25 mm/second) a

116

116

Practice * MARCH ~~~~~~~~~~~~~~~~~~~In

2002

therefore, obtaining an artefact-free tracing is important in order to clearly identify the ECG complexes. Sinus arrhythmia In the case of sinus arrhythmia, the stimulus originates from the sinoatrial node, but the rate varies (increases and decreases) regularly. This is usually associated with the variation in autonomic tone which is often synchronous with respiration and is therefore sometimes called respiratory sinus arrhythmia.

CLINICAL FINDINGS The heart rhythm varies with some regularity, increasing and decreasing in rate, and there is a pulse for every heartbeat. ECG FEATURES The ECG shows a normal P wave followed by normal QRS and T waves. The rhythm varies in rate, often associated with respiration. The rhythm is sometimes described as being regularly irregular (ie, the variation in rate is fairly regular). The rate is normal for age, breed and species.

Sinus tachycardia In the case of sinus tachycardia, the sinoatrial node generates an impulse and depolarisation which occurs faster than normal. CLINICAL FINDINGS The heart rate is faster than normal for age and breed with a pulse for every heartbeat (although with a very fast rate, the pulse may become weaker).

ECG FEATURES The ECG shows a normal sinus rhythm but at a faster rate than normal. Sinus bradycardia In the case of sinus bradycardia, the sinoatrial node generates an impulse and depolarisation which occurs more slowly than normal. This can be a normal feature in some giant-breed dogs and in athletically fit animals.

CLINICAL FINDINGS The heart rate is slower than normal for age and breed, with a pulse for every heartbeat. ECG FEATURES The ECG shows a normal sinus rhythm but at a slower rate than normal.

ABNORMAL ELECTRICAL ACTIVITY OF THE HEART

Dysrhythmia literally means abnormal rhythm; arrhythmia is a synonymous term. Dysrhythmias include abnormalities in rate, conduction or those associated with ectopia (see box below). Dysrhythmias that are essentially slow are referred to as bradydysrhythmias, and those that are fast are termed tachydysrhythmias. While there can be considerable variation in the 'normal' morphology of a QRS complex for a particular animal, it is nevertheless important to identify from the ECG recording a normal sinus complex for the animal being examined. Once a normal complex has been identified, the shape of the QRS complex and the T wave should be noted. Depolarisation of the ventricles occurs by conduction from (or through) the atrioventricular node to produce this QRS complex and it is therefore of paramount importance in any tracing to determine which shape represents the conduction that has arisen via the atrioventricular node, especially if there are a variety of shapes of QRS complexes.

Ectopia Ectopia literally means 'in an abnormal place'. In connection with the heart, this refers to outside the sinoatrial node, the dominant pacemaker. Ectopic beats arise as a result of various mechanisms due to a number of causes (eg, cardiac pathology, hypoxia,

electrolyte imbalances).

QRS

T ECG from a dog showing sinus tachycardia at a rate of 200/minute. (Lead 11, 1 cm/mV, 25 mm/second)

QRS

11

:

*

*

*

f

~~~~~~~~~~~~~4

ECG from a dog showing sinus bradycardia at a rate of 30 to 40/minute. (Leads

In Practice 0 MARCH 2002

11

and

111,

cm/mV, 25 mm/second)

117

_-s,

MORPHOLOGY OF AN ECTOPIC VENTRICULAR DEPOLARISATION

Terminology

Providing a normal QRS-T wave has been correctly tound and identified, any QRS-T complex which is not associated with a preceding P wave, and is a different shape to this normal QRS-T wave, represents an abnormal complex. When the QRS-T complex is different from the normal sinus complex, the only possible site of origin is a ventricular ectopic focus as there is no other site which can stimulate the ventricles. In addition, these ventricular ectopic complexes are not associated with a preceding P wave (unless by coincidence). The direction of the ventricular depolarisation in an ectopic case is different from that which would have occurred from depolarisation arising from the atrioventricular node. In the example shown in the diagram on the right, the ventricular ectopic depolarisation wave is travelling away from the positive electrode and is therefore displayed on the ECG paper below the baseline (ie, the QRS complex is negative). Also, because conduction has not travelled through the normal (fast) electrical conduction tissue (ie, it has depolarised the ventricular muscle mass from 'cell to cell'), the time it takes to depolarise the ventricles is prolonged. Therefore, not only is the QRS complex of the ventricular ectopic ditferent in shape, but

With an understanding of the terminology used, the interpretation of dysrhythmias due to ectopia becomes relatively easy. The term 'beat' implies that there has been an actual contraction. In 'ECG speak', it is better to use the term complex or depolarisation to describe waveforms on the ECG. Ectopic complexes may be classified by the following: * SITE OF ORIGIN. Complexes may be either ventricular or supraventricular in nature

TIMING. Ectopic complexes that occur before the next normal complex would have been due are termed premature; those that occur following a pause, such as a period of sinus arrest or in the case of complete heart block, are termed escape complexes * MORPHOLOGY. If all the ectopics in a tracing have a similar morphology to each other, they are referred to as uniform; ectopics with different shapes are known as multiform * NUMBER OF ECTOPICS. Premature ectopic complexes may occur singly, in pairs or in runs of three or more; the last is referred to as tachycardia. Tachycardia may be continuous, in which case it is known as persistent or sustained, or may be intermittent, which is termed paroxysmal * FREQUENCY. The number of premature ectopic complexes in a tracing may vary from occasional to very frequent. When there is a set ratio, such as one sinus complex to one ectopic complex, this is known as bigeminy; when there is one ectopic to two sinus complexes, this is termed trigeminy *

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ECG (lead 11) from a 10-year-old dog showing an underlying sinus rhythm interrupted by one ventricular premature complex (VPC)

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ECG (lead 11) from a cat showing an underlying sinus rhythm interrupted by an occasional ventricular premature complex

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ECG (leads I and 11) from a dog showing alternating sinus complexes with ventricular premature complexes (so-called ventricular bigeminy)

1 18

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In Practice

MARCH 2002

A ventrricular ectopic complex can occur quickly (or early), in vwhich case it is termed a ventricular premature complex. IIf a ventricular ectopic occurs after a pause (or with delay ) then it is referred to as a ventricular escape complex.

T

Ventricul lar premature complexes Ventricula r premature complexes are a common finding in dogs an d cats and arise from an ectopic focus or foci within the ventricular myocardium. Depolarisation therefore occurs in an abnormal direction through the myocardiuim and the impulse is conducted from cell to cell (not wiithin the conduction tissue).

t QRS An ectopic focus with the spreading out of the depolarisation wave (right) and

> I,

the formation of a QRS-T complex (left) associated with the ventricular ectopic. Note that because the depolarisation wave is travelling away from the positive electrode, the QRS is displayed as a negative complex on the ECG. Reproduced with permission from Blackwell Science

it is also prolonged. A useful tip is that, quite often, the T wave following a QRS complex of a ventricular ectopic is opposite in polarity to the QRS wave and large. Ventricular ectopic complexes can arise from any part of the ventricles. The direction in which they depolarise the ventricles is therefore variable, which means that the electrical potential difference recorded by the ECG will also be variable. In other words, as the direction in which the depolarisation wave travels in relation to the positive electrode is variable, the shape and magnitude of the QRS complex of a ventricular complex will also be variable. It is important to note that the QRS wave of a ventricular ectopic complex is different to the one that has arisen from the atrioventricular node and travelled normally down the electrical conducting tissue to the ventricles.

CLINICAL FFINDINGS OccasionalLI premature beats will sound like a 'tripping in the rhythnrn'. Depending on how early the beat occurs, the 'extra' 'premature beat may be heard or it might be 'silent', p roducing a brief pause in the rhythm. There b will be liti tle or no pulse associated with the premature beat (ie, a pulse deficit). If the premature beats are more frequent, tl:he tripping in the rhythm will start to make the heart rhytl hm sound more irregular. With very frequent premature beats, the heart rhythm can sound quite chaotic and, witth a pulse deficit for each premature beat, the pulse rate will be much slower than the heart rate. During a s,ustained ventricular tachycardia, however, the heart rhythim will sound fairly regular- pulses will probably be palpable, but reduced in strength, becoming weaker wilLth faster heart rates. ECG FEATIURES The QRS ecomplex morphology is abnormal (ie, unlike a QRS wave that would have arisen from the atrioventricular node). The complex is usually: * Abnormnal (bizarre) in shape; * Slightly widened (prolonged); * The T wave of a ventricular premature complex is often large and opposite in direction to the QRS wave. When aa ventricular premature complex is so premature that it is superimposed on the T wave of the precedvPCs

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ECG (leads 1, 11 and 111) from a dog showing a short burst of ventricular premature complexes which are of different shapes. This is known as multiform paroxysmal ventricular tachycardia

119

QRS QRS

ECG from a dog showing the phenomenon of R-on-T. This is where a ventricular premature complex occurs so early that it is superimposed on the T wave of the preceding ventricular premature complex

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i

f

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ECG from a dog showing only one normal sinus complex; the rest are all ventricular premature complexes (occurring at a rate of 200/minute). This is known as ventricular

-

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W

i

-

Q~RS

tachycardia

inT comi1plex (sinus

or

ectopic),

such

that the ventricles

depolairised before they haxve comipletely repolarised from the preceding contraction, this is term-ied R-on-T. A runi of three or more ventriCular premlature complexes

are

is

knows

as

ventricular tachycar-dia.

MORPHOLOGY OF AN ECTOPIC SUPRAVENTRICULAR DEPOLARISATION Any ectopic stimulus arisinig above the ventricles is reterred to as Supraventricular and can be divided into: * Those which occur in the atrial muscle mass (atrial ectopics); and * Those which arise firoIml within the atriovenitricular node or bunldle ot His (junctional or nodal ectopics). In-espective of where supraventricular ectopics arIise, they musit traxvel down the bundle ot His and so depolarise the ventricles as normal. Therefore, the morphology of the QRS complex associated with a supraventricular ectopic

the QRS complex is usually norm-i'al - thalt is, the samile for a siinus coImlplex (the exception being when there is (aberrancy). This can make identificcation of a supraventriculalr- ectopic difficLult. In the v ast majority of cases, howa premature belt, which means that it is ecer, it OCCurIs primnartily recognised by its prematue timi-ng. The QRS of a supraxventricular ectopic complex is the sarme shape as QRS of normal sinus com1lplex and is recognised by its premature timinlg and, usually, also by the absenice o' as

as

a

a

a

normal

P

\waxe.

While the timillg (in relation to its QRS complex) anld the morphology of the P axve (whichi iS usually differenit from a norm-lal P waxve) can aLid in identifying whether the ectopic alrose from the atrial (atrial preImatule coImlplex) or the atrioxentricular node (junctional or nodal premlaL.ture complex). it is initially of little practical importcance in smlall anim-Ials. In addition, it does not affect the managecrlemnt or treatmiienit in the vast major-ity of cases in smlall animials. Therefore, the distinctioln w

atriatl anid junctionial prematul-e coImIplexes not be discussed in this article aind both will be referr-ed to by the broader term. supravxentricular premnatli-e comiiplexes.

between will

Supraventricular premature complexes Suprax entricular premntature complexes arise

romio

1

an

aboxve the xventricles - that is. either in the atria, the atrioxventriculaIr node or the bundle of' His. The xventricles are thein depolarised normally, hence producing a normnal shaped QRS complcx with a normal

ectopic tOCuS

The site of origin of supraventricular and ventricular \ ectopic complexes. APC, atrial

premature complex; JPC, junctional premature complex; VPC, ventricular premature complex. Reproduced with permission from Blackwell Science

120

or

foci

durationi. CLINICAxI FINDINCiS is not possible to distinguish supraventricu lar premiatLtre beats fromi xventricular premnatul-e beats. Occasional premn-ature beats will sounld like aI 'trippinl in

Clinically, it

In Practice

MARCH 2002

~~~~~~QRS

I

QRS QR

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ECG from

a

dog showing

premature timing and

single supraventricular premature complex, recognised by preceding P wave

a

its normal QRS

morphology

but

identifiable

no

I

IQRS

I

-I~

tQRS

QRS

ECG from a dog showing a single supraventricular premature complex. On this occasion, there is a recognisable preceding P wave, which has an abnormal morphology compared to the other P waves - suggesting that this is an atrial premature

complex QRS

QRS

QRS54

T~~~~R

T

T~~~~~ ECG from

a

dog showing

a

short burst of

this is termed

supraventricular premature complexes

paroxysmal

supraventricular tachycardia

QRS

ECG from a

a

sustained

dog showing run

of

supraventricular premature \J\complexes (at a rate of in

te )

th is

~~~~~~~~~~~~~~~~~~~~~~~~~Supraventricular

rhythm',

the

with little

or

no

associated with the

pulse

premature beat. If the premature beats

tripping

the

rhythm

sound

rate

During

a

a

pulse

irregular.

With very

will

probably

becoming

be

much

sound

quite

pre-

chaotic

than

slower

the

heart

supraventricular tachycardia,

rhythm be

can

frequent

deficit for each premature beat, the

sustained

ever, the heart

will

more

frequent,

will start to make the heart

beats, the heart rhythm

mature

and, with

pulse

rhythm

in the

are more

will sound

palpable,

rate.

how-

fairly regular- pulses

but

reduced

in

strength,

P

waves

If P

may

waves

may not be identified;

or

are

they

seen,

morphology (ie, non-sinus) differ from that A

of three

run

complexes which is can

be

is

in

a

high

abnormal

an

interval

may

complex.

supraventricular premature

in

excess

400/minute)

tachycardias

of

P-R

supraventricular tachycardia,

a

at a rate as

usually

and the

normal sinus

more

or

termed

usually as

ventricular sinus

seen

are

of 160/minute (but

regular.

and

need to be

Supra-

distinguished

from

tachycardia.

weaker with faster heart rates. Atrioventricular dissociation

ECG

The term atrioventricular dissociation describes the situ-

FEATURES

QRS-T

complexes,

are seen

to occur

Normal

which have

prematurely.

a

normal

morphology,

The ECG features

are:

QRS morphology (except with bundle branch

block); The

ation when the atria and ventricles

accelerated

junctional

or

ventricular

atrioventricular conduction

QRS complex is

InPractice

MARCH

seen

200212

to occur

prematurely;

are

separate, independent foci. This may

or

depolarised

occur

rhythm,

depressed

due

to

hy an

disturbed

sinoatrial nodal

function.

121

is te

d

tachycardia

ECG from a dog showing atrioventricular dissociation. Note how the P waves (arrowed) appear to drift in and out of the QRS complexes

CLINICAL FINDINGS

The heart rhythm will sound fairly normal and the pulse should match the heart rate.

originates above the ventricles, it as a supraventricular arrhythmia.

can also be classified

CLINICAL FINDINGS ECG FEATURES

The ECG shows a ventricular rate that is usually very slightly faster than the atrial rate. The P waves may occur before, during or after the QRS complex. The P waves and QRS complexes are independent of each other, with the QRS complexes appearing to 'catch up' on the P waves. Atrioventricular dissociation should be differentiated from complete heart block. In the case of heart block, the ventricular rate is slow and much lower than the atrial rate; in atrioventricular dissociation, the atrial and ventricular rates are not dissimilar (and usually at a normal or faster rate). Atrial fibrillation Fibrillation means rapid irregular small movements of fibres. In atrial fibrillation, one of the most common arrhythmias seen in small animals, depolarisation waves occur randomly throughout the atria. As atrial fibrillation

QRS

T

ECG from

a

dog showing atrial

The heart rhythm sounds chaotic and the pulse rate is often half the heart rate, especially with fast atrial fibrillation. This is a very common arrhythmia in dogs and can be strongly suspected on auscultation by its chaotic rhythm and 50 per cent pulse deficit. Very frequent premature beats (ventricular or supraventricular) can mimic it. ECG FEATURES

The QRS complexes have a normal morphology (similar to that of supraventricular premature complexes, described above) and occur at a norm-al to fast rate. The ECG features are: * Normal QRS morphology (except when there is bundle branch block); * The R-R interval is irregular and chaotic (note this is easier to hear on auscultation!); * The QRS complexes often vary in amplitude;

QRS

T~~~~~~~~~~~( fibrillation with

a

ventricular response rate of 160/minute. Note the normal

(or supraventricular) morphology of the QRS complexes, the chaotic hear

on

auscultation) and the absence of

R-R intervals

(this is actually easier

to

P waves

Q?RS

,~~~~

III

~~~~Vwv

A\~~~~~~~~~~~

ECG from a dog showing atrial fibrillation with a ventricular response rate of nearly 300/minute

122

122

Practice * MARCH 2002 ~~~~~~~~~~~~~~~~~~~In

Escape rhythms When the dominant pacemaker tissue (usually the sinoatrial node) fails to discharge for a long period, the pacemaker tissue with a slower intrinsic rate (junctional or ventricular) may then discharge and 'escape' control of the sinoatrial node. This is commonly seen in association with bradydysrhythmias (eg, sinus bradycardia, sinus arrest, atrioventricular block). If escape rhythms did not develop, no electrical activity of any kind would occur; this is termed asystole. It is a terminal event unless electrical activity returns (hence, escape complexes are sometimes referred to as rescue beats). Ventricular standstill occurs if no escape rhythms develop during complete heart block (ie, there are P waves but no QRS com-

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plexes). Again, if ventricular electrical activity does not return, death is imminent. Junctional escapes are fairly normal in shape (ie, junctional ectopic), whereas ventricular escapes are abnormal and bizarre (ie, ventricular ectopic). A continuous junctional escape rhythm occurs at a rate of 60 to 70/minute and a continuous ventricular escape rhythm occurs at a rate of less than 50/minute. Both types of escape rhythm may be seen in complete atrioventricular block. As escape rhythms are rescue beats, they should not be suppressed by any form of treatment. Treatment should be directed towards the underlying bradydysrhythmia.

,

,

ECG showing ventricular fibrillation. Note the random unorganised deflections

* There are no recognisable P waves preceding the QRS complex; * Sometimes, fine irregular movements of the baseline - known as 'f waves' - are seen as a result of the atrial fibrillation waves. However, frequently these f waves are indistinguishable from baseline artefact (eg, muscle tremor) in small animals. Ventricular fibrillation Ventricular fibrillation is nearly always a terminal event associated with cardiac arrest. The depolarisation waves occur randomly throughout the ventricles. There is therefore no significant coordinated contraction to produce any cardiac output. If the heart is visualised or palpated, fine irregular movements of the ventricles are evident and likened to a 'can of worms'. Ventricular fibrillation can follow ventricular tachycardia. CLINICAL FINDINGS No heart sounds are heard. No pulse is palpable. ECG FEATURES The ECG shows coarse (larger) or fine (smaller) rapid, irregular and bizarre movement with no normal waves or complexes. Acknowledgement This article is based on material published in the author's book entitled 'Small Animal ECGs: An Introductory Guide' (2000), Oxford, Blackwell Science, and is reproduced with permission of the publisher. Further reading DARKE, P., BONAGURA, J. D. & KELLY, D. F. (1996) Color Atlas

of Veterinary Cardiology. London, Mosby-Wolfe FOX, P. R., SISSON, D. & MOISE, N. S. (1999) Textbook of Canine and Feline Cardiology. Philadelphia, W. B. Saunders KITTLESON, M. D. & KIENLE, R. D. (1998) Small Animal Cardiovascular Medicine. St Louis, Mosby LUIS FUENTES, V. & SWIFT, S. (1998) Manual of Small Animal Cardiorespiratory Medicine and Surgery. Cheltenham, BSAVA MARTIN, M. (2000) Small Animal ECGs: An Introductory Guide. Oxford, Blackwell Science

In Practice * MARCH 2002

MARTIN, M. & CORCORAN, B. (1997) Cardiorespiratory Disease of the Dog and Cat. Oxford, Blackwell Science SMITH, F. W. R. & TILLEY, L. P. (1992) Rapid Interpretation of Heart Sounds, Murmurs, and Arrhythmias. Philadelphia, Lea & Febiger TILLEY, L. P. (1992) Essentials of Canine and Feline Electrocardiography: Interpretation and Treatment, 3rd edn. Philadelphia, Lea & Febiger TILLEY, L. P. (1992) Self Assessment: Small Animal Arrhythmias. Philadelphia, Lea & Febiger

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