electrocardiography and its importance in dogs

7/15/2019 Electrocardiography and Its Importance in Dogs

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Chir ag M. Bhadesiya, Electrocardiography and its Importance in Dogs November 7, 2012

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INTRODUCTION

Electrocardiography is the recording at the body surface of electrical fields generatedby the heart.

Electrocardiograph is a record of the average electrical potential generated in the heartmuscles and graphed in terms of voltages and time during the different phases of cardiac

cycle.

Specific waveforms generated on electrocardiograph represent stages of myocardialdepolarization and repolarization.

Electrocardiography is a basic, valuable and easy to acquire initial test of choice in thediagnosis of arrhythmias and may also yield information regarding chamber dilation and

hypertrophy. Although interpreting an ECG may seem to be at first glance a complicated

and time-consuming task, the final interpretation and consequently the clinical utility of

the ECG data, must always be evaluated in the context of other data related to the clinical

cardiac problem. (DiFruscia et al., 1991)

Indications:

ECG is recorded when an arrhythmia is detected during physical examination (includingbradycardia, tachycardia or irregularity in rhythm).

Animals presenting with a history of syncope or episodic weakness may have cardiacarrhythmias, and an ECG is indicated in these cases. Arrhythmias in such cases may be

transient and in some cases, long-term electrocardiographic monitoring is warranted.

Arrhythmias often accompany significant heart disease and may significantly affect theclinical status of the patient and hence an ECG should be recorded.

To monitor efficacy of antiarrhythmic therapy and to determine whether arrhythmias mayhave developed secondary to cardiac medications (e.g., digoxin).

Significant arrhythmias may also occur in animals with systemic disease, including thosediseases associated with electrolyte abnormalities (hyperkalemia, hypercalcemia, and

hypocalcemia), neoplasia, gastric dilatation-volvulus, and sepsis.

(Tilley and Smith Jr., 2008)

Principles of ECG:

1) A lead consists of the electrical activity measured between a positive electrode and anegative electrode.

2) Electrical impulses with a net direction toward the positive electrode will generate apositive waveform or deflection.

3) Electrical impulses with a net direction away from the positive electrode will generate anegative waveform or deflection.

4) Electrical impulses with a net direction perpendicular to the positive electrode will notgenerate a waveform or deflection (isoelectric).

5) Standard electrocardiographic lead systems are used to create several angles ofassessment. A single lead would provide information on only one dimension of thecurrent (e.g., left vs. right). Two leads would allow two-dimensional information (e.g.,


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left vs. right and cranial vs. caudal). As many as 12 leads may be acquired

simultaneously.

6) Leads I, II, and III are bipolar limb leads. These are termed bipolar because theelectrocardiogram is recorded from two specific electrodes.

7)

Leads aVR, aVL, and aVF are augmented unipolar leads. To generate these, twoelectrodes are electrically connected (as a negative electrode) and compared with the

single electrode (positive). (Tilley and Smith Jr., 2008)


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HISTORY

A.17th and 18th centu ries: The harnessing of electri city, observation of its effects onanimal tissues and the discovery of Animal electricity.

1. 1600: William Gilbert, a physician to Queen Elizabeth-I,President of College of Physicians (before its Royal charter), and

creator of Magnetic Philosophy, introduced the term electrical

from the Greek word Amber for objects (insulators) that hold

static electricity.

2. 1668: Jan Swammerdam, a Dutchmans experiment on musclecontraction and nerve conduction with muscle suspended on a

brass hook inside a glass tube with water droplet to detect

movement and irritation of the nerve by a silver wire. He was

unaware of induction of small electrical charge that produced themovement of the muscle.

3. 1769: Edward Bancrof f, an American scientist suggested that theshock from the Torpedo fishes, which were often used for therapeutic reasons

during that era, is electrical rather than mechanical in nature. The idea of an electric

fish was generally not accepted.

4. 1773: John walsh, fellow of the RoyalSociety and member of parliament, obtained a

visible spark of an electric eel (Electrophorus

electricus). The eel was out of water as it wasnot possible to produce the spark otherwise.

He used thin strips of tin foil, demonstrated

his technique and won Copley medal in 1774

and 1783 for his work.

5. 1774: Mr. Squires, apothecary, gave life (i.e. recovery from sudden death) to a 3-year-old girl, Catherine Sophia Greenhill fallen from the first storey window by

applying shock to various parts of the body without any apparent success initially.

Upon transmitting few shocks through thorax, he perceived small pulsation. Soon

after, the child began to sigh and to breathe with great difficulty, vomited after 30

minutes. This was the first case using shock-therapy with no knowledge of actual

know-how.

6. 1786: Italian anatomists Lu igi Gilvaninoted that a dissected frogs leg twitchedwhen touched with a metal scalpel. He later

showed that direct contact with the

electrical generator or the ground through

an electrical conductor would lead to a

muscle contraction and interpreted the

results in terms of animal electricity.

Gilvanis name is given to thegalvanometer which is an instrument for


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measuring and recording electricity. This is essentially what an ECG is, a sensitive

galvanometer.

7. 1788: Published An essay on the recovery of the apparently dead [Annual Report1788, Humane society, London, pp. 225-244. Kite, C. An essay on the recovery of

the apparently dead].Kite

recorded use of electricity in diagnosis and resuscitationof person apparently dead. First record of cardiac defibrillation in case of drowning

treated in 1785.

B.1800 to 1895: The design of sensit ive instruments that coul d detect the smal l electri calcurr ents in the heart.

1. 1820: Johan (or Johann) Schweiggerinvented the first galvanometer and announcedhis discovery at the University of Halle on 16th September, 1820.

2. 1825: Leopoldo Nobil i, a Professor of Physics at Florence, developed an astaticgalvanometer using two identical magnetic needles of opposite polarity, either fixed

together with a figure of 8 arrangement ofwire loops or one movable needle with a

wire loop and one with a scale.

In 1827, using this astatic galvanometer, he managed to detect the flow of

current in the body of a frog from muscles to spinal cord. He detected the electricity

running along saline moistened cotton thread joining the dissected frogs legs in one

jar to its body in another jar.

3. 1838: Carlo Matteucci, Professor of Physics at the University of Pisa and student ofNobili, showed that an electric current accompanies each heart beat in the frog. He

used a preparation known as Rheoscopic frog in which the cut nerve of a frogs legwas used as the electrical sensor and twitching of the muscles was used as the visual

sign of electrical activity.

4. 1840: Dr. Golding Bird, a physician accomplished chemist and member of theLondon Electrical Society opened an electrical therapy room at Guys Hospital,

London.

5. 1843: German physiologist, Emi l Du bois-Reymonddescribed an action potentialaccompanying each muscular contraction. He detected the small voltage potential

present in resting muscle and noted that potential diminished with contraction of

muscles. To accomplish this, he had developed one of the most sensitive

galvanometer of his time. His device had a wire coil with over 24,000 turns (5 km of

wire). He devised a notation for his galvanometer which he called the disturbance

curve. O was the stable equilibrium point of astatic galvanometer needle and p, q,

r, and s (and also k & h) were other points in its deflection.

6. 1850: Bizzare unregulated actions of the ventricles (later called ventricularfibrillation) was described by Hoffaduring experiments with strong electrical currents

across the hearts of dogs and cats. He demonstrated that a single electrical pulse can

induce fibrillation.

7. 1856: Rudolph Von Koellikerand Henrich Mullerconfirmed that an electricalcurrent accompanies each heart beat by applying a galvanometer to the base and apex

of exposed ventricle.


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They also applied a nerve-muscle preparation to the ventricle and observed

that a twitch of the muscle just prior to ventricular systole and also a much smaller

twitch after systole. These twitches would later be recognized as caused by the

electrical currents of the QRS and T waves.

8.

1872: French physicistGabriel L ippmann

invented a Capillary electrometer, a thinglass of tube with a column of mercury beneath sulphuric acid. The mercury meniscus

moved with varying electrical potential observed through a microscope.

9. 1876: Mareyused an electrometer to record the electrical activity ofan exposed frogs heart.

10.1887: Physiologist Augustus D. Waller of St. Marys MedicalSchool, London published the first human electrocardiogram

recorded with a capillary electrometer from Thomas Goswell, a

technician in his laboratory.

11.1889: Dutch physiologist WillenEinthovenobserved Waller demonstrating

his technique at the First International

Congress of Physiologists in Bale. Waller

often demonstrated by using his dog

Jimmy who would patiently stand with

paws in glass jars of saline.

12.1891: British physiologist Wil li am Baylissand Edward Starling of University

College London improved the capillary electrometer. They connected the terminals to

the right hand and skin over the apex beat and showed a triphasic variationaccompanying (or ratherpreceding) each beat of the heart. These deflections were

later called P, QRS and T.

13.1893: Willen Einthoven introduced the term Electrocardiogram at a meeting of theDutch Medical Association.

C.1895 to 1999: The first accurate recording of the electrocardiogram and itsdevelopment as a cli ni cal test.

1. 1895: Einthoven using an improved electrometer and a correction formula developedindependently of Burch distinguished five deflections which he named P, Q, R, S and

T.

2. 1899: Karel F rederik Wenckebachpublished a paper on the Analysis of irregularpulses describing impairment of atrio-ventricular (AV) conduction leading to

progressive lengthening and blocking of AV conduction in dogs. This was later called

Wenckebach Phenomenon.

3. 1899: Jean-L ouis Prevost, Professor of Biochemistry and Frederic Batelli, Professorof Physiology, both of Geneva discovered that large electrical voltage applied across

an animals heart can stop ventricular fibrillation. They also reported that ventricular

fibrillation can be induced by small voltages (as 40 V).
http://www.aha.gr/Ventricular_electrocardiography/art-VentElec.ch01.fig1.3a.JPEGhttp://www.aha.gr/Ventricular_electrocardiography/art-VentElec.ch01.fig1.1.JPEG


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4. 1901: Einthoven discovered a new galvanometer for producingelectrocardiograms using a fine quartz string coated in silver. His

string galvanometer weighed 600 pounds and was in fact many

thousands of times more sensitive than other instruments.

5.

1908:Edward Schafer

of the University of Edinbergh was thefirst to but a string galvanometer for clinical use.

6. 1912: Thomas Lewis published a paper detailing his careful clinical andelectrocardiographic observation of atrial fibrillation in heart of a horse on Buford

Plain with Dr . Woordru ff, a veterinarian.

7. 1912: Einthoven addressed the Chelesa Clinical Society in London and described anequilateral triangle formed by his standard leads I, II and III later called Einthovens

triangle. The first reference in English article for abbreviation EKG.

8. 1924: Willen Einthoven won Nobel Prize for inventing the electrocardiograph.9. 1928: Frank Sanborns company converted their table model electrocardiogram

machine into their first portable version weighing 50 pounds and powered by a 6-Volt

automatic battery.

10.1934: By joining the wires from the right arm, left arm and left foot with 5000 Ohmresistors, Frank Wilson defined an indifferent electrode later called the WilsonCentral Terminal. The combined leads acted as an earth and were attached to the

negative terminal of the ECG. An electrode attached to the positive terminal then

became unipolar and could be placed anywhere on the body. Wilson defined the

unipolar limb lead VR, VL and VF where V stands for Voltage (the voltage seen at

the site of unipolar electrode).

11.1938: Ameri can Heart Associationand the Cardiac Society of the Great Br itaindefined the standard positions, and viewing of the chest leads V1-V6.

12.1949: Montana physician Norman Jeff H olterdeveloped a 75 poundback-pack that can record the ECG of the wearer and transmit the


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signal. The system later greatly reduced in size, combined with tape/digital recording

and used to record ambulatory ECGs.

13.1953: Osborn, whilst experimenting with hypothermic dogs, described the prominentJ (Junctional) wave which has often been known as Osborn wave. He found the

dogs were more likely to survive if they had a infusion of bicarbonate and supposedthe J wave was due to an injury current caused by acidosis.

14.1993: ECG recording had already become a routine practice for human clinics. RobertZalenski, Professor of Emergency Medicine, Wayne State University Detroit, and

colleagues published an influential article on the clinical use of 15 lead ECG which

routinely uses VGR, V8 & V9 in the diagnosis of acute coronary syndromes.

15.1999: Researchers from Texas showed that 12-lead ECGs transmitted via wirelesstechnologies to hand-held computers is feasible and can be interpreted reliably.


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ELECTROPHYSIOLOGY OF THE HEART

The cells of cardiac muscle differ from those of skeletal muscle in having the inherentability to contract and relax spontaneously. This myogenic rhythm is shown by small

pieces of cardiac tissue and even isolated myocytes.

The underlying mechanism appears to be based on a further specialization of thesarcolemma that permits a slow inward leakage of sodium ions.

Ventricular cells contract and relax at a lower frequency than atrial cells, but in the intactheart both are synchronized to a more rapid rhythm, generated by pacemaker tissue and

conveyed to them by a system of fibers specialized for conduction.

The anatomical arrangement of these tissues includes all modified cardiac cells. Threetypes may be distinguished morphologically from normal working cardiac cells: P

(P=Pale-staining = Primitive = Pacemaker) cells, transitional cells and Purkinje fibers.

Of all the cells in the heart, those of the sinu-atrial (SA) node generate the most rapidrhythm and therefore function as the pacemaker of the heart.

The SA node generates an electrical current by the movement of cations across the outermembranes of its cells.

Cations are pumped out of a cell in a process called polarization that results in theoutside of the cell having a more positive charge than the inside of the cell.

When gates in the cell wall are well opened, cations flow into the cell to equalize thecharge on either side of the cell membrane. This process is called depolarization

generates an electrical current, which causes heart muscles to contract.

The heart muscles automatically keeps going through the cardiac cycle of depolarization(systole) and repolarization (diastole).

When the electrical impulse passes through cardiac muscle, the muscle contracts. Unlike other muscle fibers in the body, cardiac muscles can transmit an electrical impulse

from one muscle cell to another, so electrical impulse and muscle contraction spread


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across the heart muscles like waves in pond after a stone is tossed in. Skeletal muscle, by

contrast, only contracts when it receives an electrical message from nerve tissue; it does

not receive electrical impulse from skeletal muscle cells.

In brief, the sequence of events is as follows.. 1.

After the electrical impulse is generated in the SA node in the right atrium, it spreadsin a wave across atria, causing them to contract and push blood through AV valves

into ventricles, which are relaxed.

2. The impulse generated by the SA node also travels quickly down the highway ofspecialized, fast conducting muscle fibers to the atrioventricular (AV) node.

3. The impulse conduction highway does encounter a slight delay at the AV node, whichis the only route of conduction of the electrical impulse from the atria to the

ventricles.

- The delay permits the atria to complete their systolic contraction beforeventricular systole (contraction) begins.

- If atrial & ventricular systole took place at the same time, the pressure in thecontracting ventricles would be so high that the weaker, thin-muscled atria could

not push blood into the ventricles.

4. After the delay at the AV node, the electrical impulse resumes its speedy journey, thistime through specialized fibers in the ventricles called Bundle of His & Purkinje

fibers.

5. Just as the atria begin their systolic contraction before the ventricles, they alsocomplete systole and enter the resting phase (diastole).

- When the ventricles are contracting, but the atria are relaxed, the pressure in theventricles is much higher than the pressure in the atria, so the AV valves snapshut.

- With the AV valve closed, the relaxed and expanding atria can fill the blood fromveins that supply them.

- At about the time when the atria are becoming completely full, systole comes toan end in ventricles, and they begin to relax.

- This results in the pressure in the ventricles dropping lower than the pressure inthe arteries they supply. So, the aortic and pulmonary valves snap shut. Pressure in

the ventricles also falls below the pressure in the full atria. So, the AV valves are

pulled open (and semilunar valves are closed).

- After the AV valves open, the ventricles fill with the blood from the atria (in muchthe same way as releasing the bulb of an eye dropper causes liquid from bottle to

be pulled up). Most ventricular filling is generated by the negative pressure caused

by ventricular relaxation pulling blood in from the atria.

6. Just as the pressure in the atria and the ventricles begins to reach equality due to themovement of blood from one ventricle to the other, the SA node, which depolarizes

during atrial diastole (relaxed atria, contracted ventricles), depolarize again.

7. This causes the atria to contract (ventricles will be relaxed) and forcibly push evenmore blood into the ventricles, and the cardiac cycle begins again.

(Katz, 2005)


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Relationship between cardiac cycle and development of P, Q, R, S & T deflection on an ECG


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TYPES OF LEADS

The leads which are used for recording electrocardiogram are mainly classified in 3categories based on the area/part of the body where they are to be attached.

1. Standard limb leads (I, II, III)2. Augmented leads (aVR, aVL, aVF)3. Precordial leads (V1, V2, V3, V4, V5, V6)

1. Standard limb leads: Commonly attached on limbs and are the first among the lead systems described by

Einthoven.

Leads are: I, II and III. These three leads form Einthovens Triangle'. These types of leads are commonly used in both; human and veterinary practice.

2. Augmented leads: Leads require augmentation and are derived from the same limb leads (I, II and

III).

Leads are: aVR, aVL and aVF.aVR: Positive electrode on the right arm,

aVL: Positive electrode on the left arm,

aVF: Positive electrode on the left leg.

These types of leads are commonly used in human electrocardiographic studiesbut are of limited use in routine veterinary practice. Pet clinics in many countries

have adopted using augmented limb leads for electrocardiographic studies in dogs

and cats.

3. Precordial leads: Precordial leads are placed directly on chest region and are in close proximity to

heart.

Leads are: V1, V2, V3, V4, V5 and V6. The reason behind no requirement of augmentation is their close proximity to the

heart.

These leads are commonly used in human electrocardiographic studies, especiallyelectrophysiological studies of the heart.


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LEAD SYSTEMS FORDOGS



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THE AXIAL SYSTEM

Color Placement

Red Left foreleg

Yellow Right foreleg

Green Left hind leg

Black Earthing

The hearts electrical axis refers to the general direction of the hearts depolarizationwavefront in the frontal plane.

With a healthy conducting system the cardiac axis is related to where the major musclebulk of the heart lies. Normally this is the left ventricle with some contribution from the

right quadrant of the hexa-axial reference system although +40 to +100 is considered to

be normal for dogs.

If the left ventricle increases its activity or bulk then there is said to be left axisdeviation as the axis swings round to the left. Alternatively, where the right ventricle is

strained or hypertrophied then the axis swings round to the right and right axis deviation

is said to exist.

Disorders of the conduction system of the heart can disturb the electrical axis withoutnecessarily reflecting changes in muscle bulk. (Tilley and Smith Jr., 2008)


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POSITIONING OF THE DOG FORECGEXAMINATION

Positioning the dog either on right or left sided recumbency will give the basic idearegarding electrophysiology based on developing electrocardiogram.

Mostly, in private clinics, right lateral recumbency is preferred for electrocardiographicstudies/examination.

The changes related with electrocardiogram are less affected by position of the dog andmore by other relevant factors (e.g., improper isolation between body and table, use of

other electrical equipment in area where electrocardiography is in progress etc.).

RECORDING AN ELECTROCARDIOGRAM

1. The electrocardiogram should be recorded in an area as quiet and as free of distraction aspossible.

2. Noises from clinical activity and other animals may significantly affect rate and rhythm.Any use of electrically operated equipment, such as clippers, may cause interference and

should be minimized during the electrocardiogram.

3. The patient should ideally be placed in right lateral recumbency.4. Limbs should be held perpendicular to the body. Each pair of limbs should be held

parallel, and limbs should not be allowed to contact one another.

5. The animal should be held as still as possible during the electrocardiogram. Whenpossible, panting should be prevented.

6. When dyspnea or other factors prevent standard positioning, the electrocardiogram maybe recorded while the animal is standing, or, less ideally, sitting.

7. Alligator clips or adhesive electrodes may be used. To reduce discomfort, teeth ofalligator clips should be blunted and the spring should be relaxed.

8. Limb electrodes are placed either distal or proximal to the elbow (caudal surface) andover the stifle. Electrodes placed proximal to the elbow may increase respiratory artifact.

9. Each electrode should be wetted with 70 % isopropyl alcohol to ensure electrical contact.10.Approximately three to four complete complexes should be recorded from each lead at 25

mm/s or 50mm/s. (Martin, 2007)


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THE ELECTROCARDIOGRAPH

ECG particulars and their interpretation:The P wave The depolarization wave of the auricular musculature which spreads radially

from the SA node to the AV node

The P-R segment This is a delay in the transmission of the impulse at the AV node.

The P-R interval The time required to depolarize the atrial musculature plus the delay in the

transmission of the impulse through the atrioventricular node to the beginningof the ventricular depolarization.

The QRS interval Depolarization complex of the ventricular musculature.

The S-T segment The depolarized state, or the duration of the excited state of the ventricular

musculature, or the interval of time between the completion of depolarization

and the beginning of repolarization of ventricular musculature.

The S-T interval The time from completion of depolarization of the ventricular musculature to

completion of repolarization.

The Junction J The point of junction between the QRS complex and the S-T segment is

known as the Junction J.

The Q-T interval The entire time required for depolarization and repolarization of the

ventricular musculature.

The T wave The wave of ventricular repolarization.

The U wave It is an after-potential wave which follows the T wave and is usually low in

amplitude.(Burch and Winsor, 1972)


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Normal electrocardiographic features in dogs:Heart rate Puppy: 70-220 bpm

Toy breeds: 70-180 bpm

Standard: 70-160 bpm

Giant breeds: 60-140 bpm

Rhythm Sinus rhythm

Sinus arrhythmia

Wandering pacemaker

P wave Height: 0.4 mV

Width: 0.04-0.05 s

PR interval 0.06-0.13 s

QRS complex Height: 2.5-3.0 mV

width: 0.05-0.06 s

ST segment Depression: Not more than 0.2 mV

Elevation: Not more than 0.15 mV

QT interval 0.15-0.25 s at normal heart rate

T waves May be positive, negative or biphasic.

Amplitude range 0.005-1.0 mV in any lead

Electrical axis +40 to +100



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CALCULATION OF MEAN ELECTRICAL AXIS OF THE HEART

Although depolarization waves spread through the heart in all directions, the averagedirection and magnitude is represented by the QRS complex.

If the QRS is predominantly positive (upwards), the average direction of thedepolarization waves is towards the positive electrode.

Conversely, if it is predominantly negative (downwards) then the depolarization wave ismoving away from the positive electrode.

When the QRS complex is equally positive and negative (and usually also small) then thedepolarization wave is moving at right angles to the positive electrode.

(Martin, 2007)

After obtaining an electrocardiogram from different leads, the deviation of the MeanElectrical Axis (MEA) of the heart, which is related with dilated cardiomyopathy, can be

decided using two different techniques for clinical electrocardiographical interpretation.

The limb leads look at the heart from sixdifferent directions.

The average direction and magnitude of thedepolarization wave through the ventricles is

termed the mean electrical axis (MEA) or the

cardiac axis.

As can be seen from Fig (a), in which there is anormal axis, leads I, II, III and aVF have positivedeflections and aVR and aVL are negative.

If the right ventricle becomes enlarged asillustrated (either with hypertrophy or dilation),

then the MEA swings to the right, because the

large increase in muscle mass on the right side

creates a large electrical potential difference during

depolarization.

In Fig. (b), for example, leads III and aVR becomelarge and positive.

Leads I, II and aVL become negative. Lead aVF isisoelectric in this example. This is termed a right

axis deviation.

(a)

(b)


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If the left ventricle becomes enlarged (either byhypertrophy or dilation), then the MEA swings to the

left, because the large increase in muscle mass on theleft side creates a large electrical potential difference

during depolarization.

In Fig. (c), for example, lead I becomes taller thanlead II. Lead aVL is also positive.

Leads III and aVR are negative and aVF isisoelectric. This is termed a left axis deviation.

A. Triangulation:o Using two leads from a good-quality tracing, commonly leads I and III are used to

measure the net amplitude of the QRS complex in each lead.

o In other words, measure the amplitude of the QRS complex that is positive and theamplitude that is negative.

o Subtract one (the smaller) from the otherthis is the net amplitude.o Plot this, to scale, on the hexa-axial lead system shown below. Draw perpendicular

lines from each point.

o Where the two lines meet is the direction of the MEA from the center point.o In fact, if the net amplitude in all six leads is calculated and plotted on the hexa-axial

lead system, the lines that are drawn perpendicular from each point should all meet atapproximately the same point.

.

(Martin, 2007)

(c)


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B. Eyeballing the MEA:o Using this method provides a quick system and, with practice, the MEA can often be

eyeballed to see whether it is normal or abnormal. Look again at the previous

diagrams describing right and left axes, and how the amplitude of the QRS complex

varies in leads I, II and III with these.

(i) Using all six limb leads and the hexa-axial lead system, find the lead in which theQRS complexes have the greatest (positive) net amplitude the MEA is

approximately in this direction.

(ii) Similarly, find the most negative complexes, the MEA is opposite in direction tothis.

(iii) Alternatively, find the lead in which the QRS complex is equally positive andnegative (and usually small)this is called the isoelectric lead. The MEA will be

perpendicular to this. Find which of the six limb leads is perpendicular to theisoelectric lead. If the perpendicular lead is positive, then the MEA is in that

direction. If the perpendicular lead is negative, then the MEA is in the opposite

direction to that lead.

(Martin, 2007)

CALCULATION OF HEART RATE BASED ON ECG RECORD

Calculation of the heart rate from an ECG is depending on the speed of the paper as wellas R-R interval.

(Martin, 2007)


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COMMON CARDIAC ABNORMALITIES IN DOGS

A. Arrhythmias:1) Normal sinus impulse formation

a. Normal sinus rhythmb. Sinus arrhythmiac. Wandering sinus pacemakers

2) Escape rhythmsa. Junctional escape rhythms

b. Ventricular escape rhythms (idioventricular rhythm)3) Disturbances of sinus impulse formation

a. Sinus arrestb. Sinus bradycardiac. Sinus tachycardia

4) Disturbances of supraventricular impulse formationa. Atrial premature complex

b. Atrial tachycardiac. Atrial flutterd. Atrial fibrillatione. Atrioventricular junctional rhythm

5) Disturbances of ventricular impulse formationa. Ventricular premature complexes

b. Ventricular tachycardiac. Ventricular asystoled. Ventricular fibrillation

6) Disturbances of impulse conductiona. Sinoatrial block

b. Persistent atrial standstill (silent atrium)c. Atrial standstill (hyperkalemia)d. Ventricular pre-excitatione. First, second and complete or third degree AV block

7) Disturbance of impulse formation + impulse conductiona. Sick sinus syndrome

b.

Ventricular pre-excitation & Wolff-Parkinson-Qhite syndromec. Atrial premature complexes & aberrant ventricular conduction

B. Other cardiac disorders:1) Congenital abnormalities in dogs

a. Patent ductus arteriosusb. Pulmonic & Aotric stenosisc. Atrial and venous septal defects

2) Other cardiac abnormalities in dogsa. Valvular disorders

b. Myocardial & Pericardial disordersc. Vascular disorders (Tilley and Smith Jr., 2008)


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Ventricular Premature Complexes (VPCs) followed by Atrial Premature Complexes(APCs), atrial fibrillation, complete third degree heart block are commonly prevalent

heart diseases of dogs.

(Patterson et al., 1961)

Atrial fibrillation, the most common abnormal arrhythmia of dog, is significantly higherin giant breeds, increases with age and is higher in males than females.

(Bohn et al., 1971)

Chronic valvular disease occurs with relatively greater frequency in small dogs.(Buchanan, 1977)

The electrocardiograms can be used for determination of the prognosis of dogs with atrialfibrillation.

(Boeve et al., 1984)

Middle-aged, large breed male dogs are more at risk to suffer from acquired cardiacdiseases like ventricular and atrial dilatation, atrioventricular valve thickening and

endocarditis. The mean age reported is 5.9 years.

(Bonagura and Ware, 1986)

Overall prevalence of heart diseases in dogs remains between 9.0% to 12.00% in general.(Fioretti and Delli, 1988)

Spontaneous heart diseases are more prevalent now in dogs than previously considered.The incidence of the acquired heart diseases in dogs increases with age. Acquired heart

diseases comprise the vast population, whereas the congenital heart diseases are much

less important (0.6% of a clinic population).

(Drake, 1992)

Sinus arrhythmia is the most common type of arrhythmia in dogs.(Rouholamine et al., 2000)

One in ten dogs has a heart disease.(Dove, 2001)

The most commonly affected breeds for cardiac diseases in India are cross breed dogsfollowed by Pomeranians.

(Vengsarkar, 2001)

Atrial standstill, a rare electrocardiographic change is associated with hyperkalemia whenthe serum potassium (K) level is greater than 8.5 mEq/L and characterized by absence of

P wave.

(Jeyaraja et al., 2004)

The ECG has been considered as sensitive indicator of changes in plasma concentrationsof calcium and potassium ions and a poor indicator of abnormal concentration of sodium

and hydrogen ions.

(Surawicz, 1967)

The calcium deficiency can lengthen the Q-T interval, while an increase in the levels ofcalcium ions and decrease in potassium ions are associated with a flattening and inversion

of the T wave.

(Symonds, 1971)


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Gujarat: Out of 1095 dogs screened and overall prevalence of cardiac diseases wasrecorded as 7.67% which included

- Cardiac arrhythmias : 63.1%

- Cardiomyopathy : 16.7%

- Heart worm : 8.3%(Sarita Devi et al., 2011)

Overall Prevalence of Different Cardiac Diseases reported in Gujarat:

(Sarita Devi et al., 2011)

Age-wise Prevalence of Different Cardiac Diseases reported in Gujarat:

(Sarita Devi et al., 2011)


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ABNORMAL ELECTROCARDIOGRAM

Sr.

No.Condition ECG & Interpretation

1. Sinus rhythm

Normal P wave followed by QRS-T waves Rhythm: Constant or regular Rate:Normal

2.Sinus

arrhythmia Normal P wave followed by QRS-T waves Often associated with respiration Rhythm: Varies (Regularly irregular) Rate:Normal

3.

Sinus

tachycardiaHeart failure

(Mitral valve

disease)

13 Year-old Dog Normal sinus rhythm but at a faster rate than normal

4.Sinus

bradycardia

Normal sinus rhythm but at a slower rate than normal(Martin, 2007)


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5.

Ventricular

PrematureComplex (VPC)

Abnormal QRS morphology (bizarre, wide/prolonged) T wave is often large and opposite in direction to the QRS complex

6.

Ventricular

tachycardiaNegative QRS

morphology

One normal sinus

complex (green

arrow)(10 year-old

Labrador, liver

neoplasia)

7.

Supraventricular

Premature

Complex Normal QRS morphology. QRS occur prematurely. P wave may or may not be identified. If P wave is identified, it will be of abnormal morphology. P-R interval will differ from a normal sinus complex.

8.

Ventricular

escape complex(Following the long

flat line) Bradycardia. SA node fails to discharge for longer period and other pacemaker tissue may

then discharge or escape the control of the SA node.

(Martin, 2007)


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9.AV dissociation(6 year-old

Labrador) Ventricular rate is faster than atrial rate. P wave may occur before, during or after QRS complex. P wave & QRS complexes are independent of each other with the QRS

complex appearing to catch-up on P waves.

10.Atrial

fibrillation Normal QRS morphology. P-R interval irregular and chaotic. QRS complexes often vary in amplitude. No recognizable P waves preceding QRS complexes. Some irregularity on baseline due to fibrillation: f waves.

11.Ventricular

fibrillation ECG will show coarse (larger) or fine (smaller), irregular and bizarre

movement with no normal wave or complex.

12. Sinus arrest

Pause in rhythm with neither P wave and therefore the QRS-T complex, i.e.,the baseline is flat.

Presence of flat line may be followed by escape complexes. Pause twice the R-R interval = Sinus block. Pause more than twice the R-R interval = Sinus arrest.

(Martin, 2007)


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13.

Sick sinus

syndrome Quite variable features. Persistent sinus bradycardia or episodes of sinus arrest without escape beats. There is failure of rescue escape beats and there can be presence of alternating

supraventricular tachycardia.

14. Atrial standstill Absence of P waves. Usually with a slow escape rhythm. QRS complexes are often of a relatively normal shape, but sometimes of

prolonged duration.

15.First degree AV

block P and QRS complexes are of normal configuration. Only P-R interval is prolonged. Delay in conduction with normal sinus rhythm.

16.

Second degree

A-V Block(9 year-old

Labrador) P wave is normal but, there is either an occasional or frequent failure of

conduction through the AV node resulting in absence of QRS complex.

If P-R interval increases prior to block: Mobitz type-I block If P-R interval remains constant prior to block and frequency of the block is

frequent: Mobitz type-II block

(Martin, 2007)


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17.

Complete/3rd

Degree AV

block+ Ventricularescape rhythm of45/min

(9 year-old

Labrador) P wave occurs at regular and a faster rate. The QRS-T complexes are at a much slower rate and usually fairly regular. The P wave and QRS complexes occur independently of each other.

18.

Complete/3rd

Degree AV

block

+ Ventricularescape rhythm of30/min

(10 year-old Collie)

19.Wandering

pacemaker

P waves can vary in morphology. Variation in amplitudes, varying from positive, negative or biphasic, or they

can even be isoelectric.

20. Left atrialenlargement

P wave is often prolonged and sometimes also notched. This is due to asynchronous depolarization of atria, the dilated left atrium

depolarizing fractionally later than right atrium.

P wave prolonged + notched = P-mitrale(Martin, 2007)


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21.Right atrial

enlargement

P wave is increased in amplitude. Tall P wave are referred to as P-pulmonale.

22.Left ventricular

enlargement

Tall R waves. Prolonged QRS duration. Shift in MEA to left.

23.

Right

ventricular

enlargement

Deep S waves. Prolonged QRS duration. Shift in MEA to right.

(Martin, 2007)


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29

24.Electrical

alternans

Alteration in QRS amplitude that occurs nearly every other heart beat. Possibly due to pericardial effusion which leads to change in cardiac axis due

to movement of the heart.

25. Pericarditis

S-T segment abnormality/elevation along with electrical alternans (differentQRS amplitude).

26. GDV

Ventricular arrhythmias occur in GDV 12 to 72 hours after onset. Sometimes ECG shows VPCs. One of the important causes include myocardial ischemia.

27. Hyperkalemia

Progressive bradycardia. Increased amplitude of T wave, appearing narrow and spiked. Progressive reduction in amplitude of P and R wave morphologies. Disappearance of P waves occurs later, i.e., atrial standstill and finally it can

terminate to ventricular fibrillation and asystole.

(Martin, 2007)


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CONCLUSIONS

Heart diseases in dogs is a significant disease entity as a cause of morbidity; it must betherefore taken into account during routine examination of dogs.

ECG is a basic, valuable, easy to acquire, initial test for diagnosis of cardiac diseasesincluding chamber dilatation and hypertrophy. Impulse conduction may or may not change heart rhythm. ECG is essential to aid cardiac

evaluation to establish a cause, an anatomic & physiologic diagnosis and a prognosis.

The perioperative evaluation and monitoring of cardiac activity by using ECG is veryimportant for dogs.

Standard leads (I, II and III) as well as augmented leads (aVR, aVL and aVF) are used forelectrocardiography in dogs.

The mean electrical axis (MEA) helps in identifying cardiac dilatation and muscularhypertrophy.

Breeds predisposed to cardiac disorders include cross-bred dogs followed by Pomeranianin India.

Cardiac arrhythmias can be diagnosed by using ECG when the P waves are examined incomparison to the QRS complexes.

Sinus arrhythmia is the most common type of arrhythmia in dogs and is a result ofvariations in vagal tone in dogs.

T wave is often large and in opposite direction to the QRS complex in VPCs. Atrial fibrillation is significantly higher in giant breeds, increases with age and is higher

in males than females and is characterized by presence of f waves.

There will be absence of any wave or deflection in ventricular fibrillation. Flat line on ECG with twice the R-R interval indicates sinus block and more than twice

the R-R interval indicates sinus arrest.

Absence of P waves with presence of slow escape rhythms on ECG indicates atrialstandstill.

Sustained absence of P wave is observed in atrial standstill while sinus arrest producesintermittent flat lines.

First degree AV block is characterized by prolonged P-R interval. Increased P-R interval before second degree AV block indicates Mobitz type-I while

constant and frequently appearing P-R interval before the block indicates Mobitz type-IIAV block.

Presence of tall R waves on ECG and deviation of MEA towards left side indicates leftventricular hypertrophy while Presence of deep S waves on ECG and deviation of MEA

towards right side indicates right ventricular hypertrophy.

ECG is sensitive indicator of changes in plasma concentrations of calcium and potassium.ECG is a poor indicator of abnormal concentrations of sodium and hydrogen ions.

Increased, narrow and spiked T wave indicates hyperkalemia, a condition which furthercan lead to atrial standstill and asystole.


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FUTURE PERSPECTIVE

There is no doubt that electrocardiography is an indispensable tool in numerous

emergency situations to monitor cardiac rate and rhythm such as cardiac arrest,

myocardial trauma in hit-by-car accidents, acute malignant cardiac arrhythmias, andintensive care or anesthetic monitoring for high-risk patients. For identifying electrolyte

and acid-base disorders, changes in the ECG (P wave, PR interval, ST segment, QRS

duration, QT interval, etc.) are usually relatively nonspecific and very vague to the point

that the value of this diagnostic aid is very low. In future, following aspects can be

considered related with electrocardiography.

1. Use of electrocardiography with microphone, i.e., Phonocardiography can provideconsiderable information on heart sounds additional to that acquired by examination with

stethoscope.

2. Use ofHolter monitor can be advised to owners and the ECG obtained by that machineshould be interpreted by veterinarians for ambulatory monitoring of cardiac activity of

dogs.
http://en.wikipedia.org/w/index.php?title=File:Wiggers_Diagram.svg&page=1


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32

3. Use of ECG software for teaching/education, research as well as at clinics should beencouraged.

Besides these all, in India, a ready format for the use of electrocardiography routinelymay be prepared and used at pet clinics in future.

This may include details of the animal & owner (for future therapeutics & management),clinical history & clinical observation especially in relation with suspected cardiac

abnormality, space for interpretation of electrocardiographic features, area to calculate

mean electrical axis (MEA) for that particular patient and a space where printed

electrocardiograph can be pasted.

In future, this can be an aid for research works as well as to maintain records on cardiacdisorders prevalent in dogs and therapeutic management of such diseases diagnosed by

use of electrocardiography. For example, a simple format is shown below.

ECGre

cord/minute


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Interpretation of ECG

Name of owner: _____________________________________________________________

Adress: ____________________________________________________________________

Contact No.:_________________________________________________________________

Animal:

Breed: _____________________________________________________________________

Age: ______________________________________________________________________

History:

Clinical findings related with suspicious cardiac disorder:

Auscultation:

Pulse rate:

ECG findings: Paper speed ____________________________

Particulars Findings Remarks

P wave Amplitude:

Duration:

QRS

complex

Amplitude:

Duration:

T wave Amplitude:

Duration:

P-R segment

P-R interval

S-T segment

S-T interval

J wave

Q-T interval

U wave

P-P interval

R-R interval


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Heart rate calculated from ECG tracing:

Mean Electrical Axis (MEA):

MEA interpretation:

ECG:

Signature


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REFERENCES:

Bohn, F. K., Patterson, D. F. and Pyle, R. L. (1971). Atrial fibrillation in dogs. Br. Vet. J.,

127: 485-496.

Bonagura, J. D. and Ware, W. A. (1986). Atrial fibrillation in the dog: clinical findings in 81

cases.J. Am. Anim. Hosp. Assoc., 22: 111-120.

Bouve, M. H., Stokhof, A. A. and Van den Brom, W. E. (1984). Prognostic significance of

the electrocardiogram in dogs with atrial fibrillation: a retrospective study of 59

cases.Res. Vet. Sci., 36: 32-36.

Buchanan, J. W. (1977). Chronic valvular disease (endocardiosis) in dogs. Advances in

Veterinary Science and Comparative Medicine, 21: 75-106.

Burch, G. E. and Winsor, T. (1972). The normal electrocardiogram. In: A Primer ofElectrocardiography, 6th Ed. Library of Congress card number-78-146022. Lea &

Febiger, Philadelphia, pp. 03-08.

DiFruscia, R., OGrady, M. and Hill, B. (1991). Diagnostic electrocardiography: When and

why should I do an electrocardiogram?. Can. Vet. J., 32: 182-183.

Dove, R. S. (2001). Nutritional therapy in the treatment of the heart diseases in dogs.

Alternative Medicine Review, 6: 38-45.

Drake, P. G. G. (1992). Doppler echocardiography.J. Small Anim. Pract., 33: 104-112.

Fioretti, M. and Delli, C. E. (1988). Epidemiological survey of dilatative cardiomyopathy in

dogs. Veterinaria., 2: 81-90.

Jeyaraja, K., Nambi, A. P., Thirunavukkarasu, P. S. and Vasu, K. (2004). Hyperkalemic atrial

standstill in a dog.Indian Vet. J., 81: 828-829.

Katz, A. M. (2005). Physiology of the heart, 4 th Ed. Lippincott Williams & Wilkins.

Baltimore.

Martin, M. (2007). Part-2: Abnormal electricity of the heart and Part-3: More advanced

electrocardiography. In: Small Animal ECGs-An introductory guide, 2nd Ed.,

Blackwell Publications, U.K., pp. 13-72.

Patterson, D. F., Detweiler, D. K., Hubben, K. and Botts, R. P. (1961). Spontaneous abnormal

cardiac arrythmias and conduction disturbances in the dog (a clinical and

pathologic study of 3000 dogs).Am. J. Vet. Res., 22: 355-369.

Rouholamine, R., Rezakhani, A. and Shirani, D. (2000). A study on electrocardiographic

parameters of normal German Shepherd dogs in Iran. J. Faculty Vet. Med. Uni.

Tehran, 53: 21-25.


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Sarita Devi, Varshney, J. P., Vagh, A. and Jani, R. G. (2011). Prevalence of cardiac diseases

in dogs of Gujarat State.Indian J. Vet. Med., 31(1): 44-45.

Surawicz, B. (1967). Relationship between electrocardiogram and electrolytes. American

Heart Journal, 73: 814-834.

Symonds, E. M. (1971). Configuration of the fetal electrocardiogram in relation to the fetal

acid-base balance and plasma electrolytes. Journal of Obstetrics and Gynecology

of the British Commonwealth, 78: 957-970.

Tilley, L. P. and Smith Jr., F. W. K. (2008). Electrocardiography. In: Manual of Canine and

Feline Cardiology, 4th Ed., Saunders-Elsevier, St. Louise, Missouri, pp. 49-77.

Vengsarkar, S. A. (2001). The diagnosis of cardiac diseases in canines. M.V.Sc. Thesis in

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India.

electrocardiography and its importance in dogs

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