ELECTROCARDIOGRAPHY IN

DOGS

Dr.K.MAHENDRAN
ECG:

 An electrocardiograph (ECG), - simplest form, is a

voltmeter (or galvanometer) that records the changing
electrical activity in the heart by means of positive and
negative electrodes

 The electrocardiogram, is a graph of the variations in

voltage produced by a mass of associated cardiac
muscle cells or bundle of muscle fibres

Electrocardiography - the process of recording these

changing potential differences
The electrocardiogram (ECG)

Records the electrical activity (depolarization and

repolarization) of cardiac muscle from the body
surface and provides information on heart rate,
rhythm, and intracardiac conduction
 HISTORY OF ECG

 Harvey – 1616 discovered that heart beats to circulate the

blood

 Augustus D.Waller 1887, reported the electrical changes

using Lipmann’s capillary electrometer in man, used the
term “electrocardiogram”

 Einthoven 1895, introduced the terms P,Q,R,S, and T

 Einthoven 1903, developed string galvanometer
“Nobel prize” in 1924

 Nurr 1922, ECG in the dog – clinical view

 Lannek 1949, systematic study and statistical

analysis of ECG – dogs – introduction of
precordial lead system
Indications and Role of the Electrocardiogram:

 Documentation of Cardiac Arrhythmias

 Assessment of Chamber Enlargement Patterns

 evidence of pericardial effusion

 to monitor efficacy of antiarrhythmic therapy

 diseases associated with electrolyte abnormalities

Limitations of Electrocardiography:

interpreted as part of the clinical picture

tells nothing about the mechanical status of the heart,

since an animal with congestive heart failure may have a
normal electrocardiogram

cannot always indicate the prognosis

does not record the pathologic features of valves,

coronary arteries, endocardium, or pericardium; only of
the myocardium

avoid trying to read too much into an

electrocardiogram if border line changes are present
 Routine approach to the electrocardiogram:

 Calculate the heart rate

 Evaluate the heart rhythm

 Measure the complexes and

intervals ( P wave, P-R
interval, QRS complex, S-T
segment, T wave and Q-T
interval)

Basic limb leads (I, II, III,

aVR, aVL and aVF)

 Determine the Mean

Electrical Axis
Electrocardiographic paper:
It is lined into boxes that can be used to make quick and
accurate measurements

There are two sets of boxes on the electrocardiographic

paper: one large and one small

Every fifth vertical and horizontal line is darker than the

others

The horizontal lines are 1mm apart and represent 0.1 mv

when the electrocardiogram is standardized at 10mm = 1
mv, ten small boxes vertically are equal to 1 mv
Electrocardiographic paper:(cont.,)
The vertical lines are time lines with each interval 0.02
sec when recorded at the standard paper speed of
50mm/sec. Five small boxes are equal to 0.1 sec

Electrocardiographic complex values of magnitude are

expressed in millivolts (mv), whereas values of duration
are expressed in seconds
PQRST deflections - Einthoven
 P wave corresponds to atrial depolarization or
contraction
 QRS wave corresponds to ventricular
depolarization or contraction
 T wave corresponds to ventricular repolarization
or relaxation
Descartes use of the letter P to designate a
point on a curve
Conducting system of the heart
Formation of P wave
Formation of Q wave
Formation of R wave
Formation of S wave
Recording of Electrocardiogram:

Area as quiet and as free of distraction as possible

Use of electrically operated equipment minimized

Placed in right lateral recumbency

Limbs should be held perpendicular to the body

limbs should not be allowed to contact one another

Recording of Electrocardiogram:( cont.,)

Alligator clips or adhesive electrodes may be used

Limb electrodes are placed either distal or proximal to

the elbow (caudal surface) and over the stifle

Electrode should be wetted with 70 % isopropyl

alcohol to ensure electrical contact

Three to four complete complexes should be recorded

from each lead at 50mm/sec
Positioning for ECG
Lead systems:
Each different angle or pair of electrodes is called a lead

Bipolar standard leads:

Leads I – Right Arm (−) compared with left arm (+)
Lead II – Right Arm (−) compared with left leg (+)
Lead III – Left arm (−) compared with left leg (+)

The 3 standard leads are bipolar (they show the activity

of the heart from two different locations)
Uses:
Studying abnormalities in P-QRS-T deflections
Diagnosing cardiac arrhythmias
Determining the MEA
 Lead systems: (cont.,)

Augmented unipolar limb leads:

It use the same electrodes, but the lead selector switch (aVR,
aVL, aVF) connects them together in different angles

The augmented unipolar limb lead compares the electrical

activity at the reference limb to the sum of the electrical
activities at the other two limbs

Leads aVR–right arm (+) compared with left arm and left leg (-)
Lead aVL – left arm (+) compared with right arm and left leg (-)
Lead aVF – left leg (+) compared with right arm and left arm (-)

Uses:
Determining the mean electrical axis or the position of the
heart
Confirming information obtained from other leads
 Augmented unipolar limb leads

aVR: aVL: aVF:

Right thoracic limb (+) Left thoracic limb (+) Left pelvic limb (+)
compared with average compared with average compared with average
voltage of left thoracic voltage of right thoracic voltage of right thoracic
limb and left pelvic limb limb and left pelvic limb limb and left thoracic
(−) (−) limb (−)
Special leads:

Unipolar precordial chest leads

CV5RL (rV2)
CV6LL (V2)
CV6LU (V4)
V10

Modified orthogonal lead systems

Lead X – lead I : right (-) to left (+)
Lead Y – lead aVF: cranial (-) to caudal (+)
Lead Z – lead V10

Invasive leads
Esophageal leads
Intracardiac leads
Unipolar precordial chest
leads:

CV5RL (rV2): Right fifth

intercostal space near the
sternum
CV6LL (V2): Left sixth
intercostal space near the
sternum
CV6LU (V4): Left sixth
intercostal space near the
costochondral junction
V10: Over the dorsal process
of the seventh thoracic
vertebra
Normal PQRST
Analysis of canine P-QRS-T deflections:

•Differentiating between normal and abnormal

•Differentiating between various abnormal

electrocardiographic patterns and their correlation with
known cardiac entities
P wave :
Represents depolarization of the atria and its duration
indicates the time required for an impulse to pass from SA
node to AV node
Height Maximum: 0.4 mV
Width Maximum: 0.04 s (Giant breeds 0.05 s)

P Pulmonale : Right atrial enlargement

P Mitrale : Left atrial enlargement
PR interval:

Normal duration: 0.06-0.13 s

Represents the time required for an impulse to travel

from SA node to the ventricle

Measured from the beginning of P wave to the beginning

of Q wave
QRS :
Represents depolarization of the ventricles. Its various
components are ( Q wave, R wave, S wave)
R Wave Height:
Large breeds: 3.0 mV maximum†
Small breeds: 2.5 mV maximum
QRS Width:
Large breeds: 0.06 s maximum
Small breeds: 0.05 s maximum

Left bundle branch block:

•Delay or block of conduction in the left bundle branch

•The left ventricle is then activated, causing the QRS complex wide and
bizarre
ECG Changes:
QRS complex > 0.08 sec
T wave:
Represents first major deflection following the QRS
complexes and represents repolarization of the ventricles

May be positive, negative, or biphasic

Amplitude range ± 0.05-1.0 mV in any lead

Not more than ¼ of R wave amplitude

ST segment:
 represents the period between ventricular depolarization and
repolarization

 Depression Not more than 0.2 mV

 Depressed ST segment: myocardial ischaemia, myocardial

infarction(subendocardial), hyperkalemia or hypokalemia
ST segment:

Elevation No more than 0.15 mV

Elevated ST segment: Pericarditis, left ventricular epicardial

injury, myocardial infarction (transmural), myocardial hypoxia
QT Interval: (0.15-0.25 sec)
total time of ventricular depolarization and repolarization
 measured from onset of QRS complex to end of T wave
Prolonged QT interval : hypocalcemia, hypokalemia, quinidine
toxicity
 Shortened QT interval : hypercalcemia, hyperkalemia, digitalis
toxicity
 Mean Electrical Axis

The electrical activity of the heart produces

simultaneously many potentials of many directions in
the three dimensional field

The electrical axis refers to the average direction of

this activation process during the cardiac cycle

Using the six limb leads and the different angles at

which they record the heart’ s electrical activity, one
can estimate the mean electrical axis in the frontal
plane
 The MEA describes the average direction of the
ventricular depolarization process in the frontal plane

It represents the summation of the various

instantaneous vectors that occur from the beginning
until the end of ventricular muscle activation

Estimation of the MEA helps the clinician identify

major intraventricular conduction disturbances and/or
ventricular enlargement patterns that shift the average
direction of ventricular activation

Normal MEA : Dogs: + 40° to + 100°

Cats: 0 to ± 160°
Estimating the Axis by major deflection:

Find the lead (I, II, III, aVR, aVL, or aVF) with the largest R
wave (note: the R wave is a positive deflection)

The positive electrode of this lead is the approximate

MEA orientation
•
Finding the isoelectric lead:

Find the lead (I, II, III, aVR, aVL, or aVF) with the most
isoelectric QRS (positive and negative deflections are
about equal). Then identify the lead perpendicular to
this lead on the hexaxial lead diagram

If the QRS in this perpendicular lead is mostly

positive, the MEA is toward the positive pole of this
lead.

If the QRS in the perpendicular lead is mostly

negative, the MEA is oriented toward the negative pole
Mean Electrical Axis:
Although depolarisation waves spread through the ventricles in
'all directions', the average direction and magnitude is represented
by the QRS complex

If the QRS is predominantly positive (upwards) the average

direction of the depolarisation waves is towards the positive
electrode.

Conversely, if it is predominantly negative (downwards) then the

depolarisation wave is moving away from the positive electrode

The average direction and magnitude of the depolarisation wave

through the ventricles is termed the mean electrical axis (or cardiac
axis)

In a normal axis, leads I, II, IIl and aVF have a positive deflection
and aVR and aVL are negative
Hexaxial system
Method for MEA:

Measuring net amplitude in lead I and net amplitude in

lead III

In triaxial system the point representing the net value

obtained is marked off from the zero point on lead I and

this procedure repeated for the sum of the deflections in

lead III

Perpendiculars are followed fromthese two points to their

intersection

A line drawn from the centre to this intersection represents

the QRS axis
BIATRIAL ENLARGEMENT
The P wave is of increased amplitude and duration
ECG changes:
• P wave is > 0.4mV and wider than 0.04 sec
• Notching and slurring of the P wave

Conditions:
Chronic mitral and tricuspid valve insufficiency, chronic mitral valve
insufficiency with pulmonary congestion, causing secondary
pulmonary hypertension and right atrial enlargement
Right Ventricular enlargement:

ECG features:
•S wave in lead CV6LL greater than 0.8mv
•S wave in CV6LU greater than 0.7mv
•S wave in lead I greater than 0.05 mv
•S wave in lead II greater than 0.35 mv
•Presence of deep Q waves in leads I,II,II, and aVF greater than 0.5mv

Associated conditions:
•Congenital cardiac defects like PS, Tetralogy of Fallot, reverse-
shunting PDA, Tricuspid dysplasia
•Heart worm disease and CHF
 Left Ventricular enlargement:
It indicate dilatation and/or hypertrophy (concentric
and eccentric)
Due to the increased muscle mass in hypertrophy,
the height of R wave is increased, the QRS complex
is delayed or altered in conduction, ST segment is
dsepressed (endocardial ischeimic channge) and
the T wave or repolarization process is changed
ECG features:
•Dogs < 2 years, the R wave should not be >
3.0mv
•Sum of lead I and III > 4.0 mv
•In older dogs R wave > 2.5mv
•The duration of QRS > 0.05 sec and 0.06 sec
•ST coving
•T wave increased

Associated conditions:
•Eccentric hypertrophy(MI, AI, VSD, PDA)
•Concentric(Aortic stenosis)
•DCM
BiVentricular enlargement:

•Simultaneous enlargement of both ventricles difficult to diagnose

•The most reliable features in man in the precordial chest leads

ECG features:
•Precordial chest leads show changes for both right (deep S
waves in CV6LL & CV6LU) and left (tall R waves in CV6LL &
CV6LU) ventricular enlargement
Left Bundle Branch Block:

It is a delay or block of conduction in the left bundle branch, the

left ventricle is activated late causing the QRS complex to become
wide and bizarre
ECG features:
•The QRS complex is of greater than 0.08 sec duration
•The QRS complex is wide and positive in leads I,II,III and aVF
•The QRS complex is inverted in leads aVR, aVL, and CV5RL
•Presence of first or second degree AV block indicate involvement of right
bundle branch
•Intermittent bundle branch block(tachycardia- or bradycardia dependant)
or bundle branch block alternans in serial tracings

Associated conditions:
•Severe underlying bundle branch disease
•Ischeimic cardiomyopathy ( arteriosclerosis of the caronary
arteries, myocardial infarction)
•Congenital Subvalvular Aortic stenosis
•DCM
Right Bundle Branch Block:
It is a delay or block of conduction in the right bundle branch, the right
ventricle is stimulated by the impulse, which passes from the left bundle
branch to the right side of the septum below the block, activated late causing
the QRS complex to become wide and bizarre

ECG features:
•The QRS complex is of greater than 0.08 sec duration
•The QRS complex has large wide S waves in leads I,II,III
and aVF, CV6LL, CV6LU
•The QRS complex is positive in leads aVR, aVL, and
CV5RL and has wide RSR’ or rsR’ pattern often M shaped
in CV5RL
•Presence of first or second degree AV block indicate
involvement of left bundle branch
•Intermittent bundle branch block(tachycardia- or
bradycardia dependant) or bundle branch block alternans
in serial tracings
Associated conditions:
•Congenital heart disease
•Chronic valvular fibrosis
•After cardiac arrest
•Cardiac neoplasia
•Chronic Trypanosoma cruzi infection
 Canine cardiac arrhythmias

Arrhythmia :
1. Abnormality in rate, regularity, or site of origin of
the cardiac impulse

2. Disturbance in conduction of the impulse such that

normal sequence of activation of the atria and
ventricles is altered
 Classification of canine cardiac arrhythmia
I.Sinus rhythm
 Normal sinus rhythm
 Sinus tachycardia
 Sinus bradycardia
 Sinus arrhythmia
 Wandering sinus pacemaker
II. Abnormalities of impulse formation:
A. Supraventricular
 Sinus arrest
 Atrial premature complexes (APC’S)
 Atrial tachycardia
 Atrial flutter
 Atrial fibrillation
B. Atrioventricular junction:
• AV junctional premature complexes
• AV junctional tachycardia
• AV junctional escape rhythm
C. Ventricular:
• Ventricular premature complexes
• Ventricular tachycardia
• Ventricular flutter, fibrillation
• Ventricular asystole
• Ventricular escape rhythm
III.Abnormalities of impulse conduction:
 Sinoatrial block
 Persistent atrial standstill
 Atrial standstill
 AV block(first degree, second degree,third degree)
 Sinus tachycardia
 Regular sinus rhythm- heart rate > 160 beats/min
 Associated conditions: exercise, fever, shock,
anaemia, infection, CHF, hypoxia, atropine,
epinephrine, vasodilators.
Sinus Bradycardia
• Regular sinus rhythm, heart rate < 70 beats/min
• Associated conditions: increased vagal tone, eyeball
pressure, elevated intracranial pressure,
hypothermia, hypothyroidism, renal failure , cardiac
arrest, CNS lesions
• Treatment : atropine or glycopyrrolate followed by IV
infusion of isoproterenol
Sinus arrhythmia

 Irregular sinus rhythm originating – SA node, alternating

slower and more rapid heart rates related to respiration
 Associated conditions: normal finding in dogs
 Wandering sinus pacemaker
A variant of sinus arrhythmia, is a shift of the pacemaker from
within the SA node or from the SA to the AV node

ECG changes:
•Gradual change in configuration of the P wave
•P-R interval constant
•QRS complexes are same
•P wave becomes positive, diphasic, isoelectric, and
negative.
 Sinus arrest
•When the SA node fails to discharge as expected, a pause in the rhythm
will occur
•The duration of the pause is at least twice the preceding R-R interval. When
severe, pause duration may be 5 to 12 seconds

Causes include fibrosis of the SA nodal tissue, greatly

increased vagal stimulation, drug influences (digoxin, beta
blockers), and rarely neoplasia
Sinus Arrest
Atrial Premature Complexes
Causes: Any disease associated
with atrial enlargement , degenerative
APC is an abnormal beat valve disease, congenital heart disease, or
occurring prematurely cardiomyopathy. Hypoxia, atrial neoplasia,
and originating in atrial tissue (ectopic and chronic obstructive pulmonary
foci) disease.

• Presence or absence of ectopic P wave & P wave - normal

morphology
• Ectopic P wave may be superimposed on preceding T
wave.
• Premature QRS with identical or nearly identical
appearance to normal QRS
APC
Atrial Tachycardia
A rapid regular rhythm originating from a focus in the atria away from the
SA node. Three or more consecutive APC’s considered to be AT.

•QRS complexes are

• Rapid rate—from 200 to 350 generally normal but may
bpm widen, or electrical
• Usually a regular rhythm. alternans may develop.
• If originating from multiple • Sudden onset and sudden
atrial sites, then an irregular termination of arrhythmia
rhythm may occur. • May occur as a reentrant
• P waves may be difficult arrhythmia within the AV
to discern. node
Atrial tachycardia originates from an abnormal atrial
focus or atrial reentry (repetitive activation from
electrical conduction around an abnormal circuit within
the atria)

P’ waves are often hidden within the QRS-T complexes

Atrial Tachycardia
 Atrial flutter results from a single (macro-) reentrant
wave of electrical activation regularly cycling through the
atria, usually at >300–400 cycles/minute

‘Sawtooth’ flutter waves, representing recurrent atrial

activation, are seen between QRS complexes on the ECG

Atrial flutter is not a stable rhythm; it often degenerates

into atrial fibrillation (AF) but may convert to sinus
rhythm
Atrial enlargement is a common underlying factor
 Atrial flutter

Rapid and regular atrial

rhythm at a rate varying
from 300-500 bpm
•F waves is regular with
Four mechanisms: Causes :
300 bpm
1. Circus movement of Atrial enlargement,
electrical impulses in a ruptured chordae
•Normal P waves
ring of tissue b/w 2 tendinae, atrial
replaced by sawtooth
veneae cavae septal defect,
flutter waves
2. Unifocal atrial impulse tricuspid dysplasia,
formation chronic mitral
•QRS is normal or wide
3. Multiple re-entry valvular fibrosis.
and bizarre
4. Multifocal atrial
impulse formation
ATRIAL
FIBRILLATION

Atrial electrical activation is rapid and chaotic

because of multiple small reentrant circuits in AF

The AV node is bombarded by these chaotic electrical

impulses; therefore, AV conduction velocity and
recovery time determine the (ventricular) heart rate

No P waves are seen on ECG because no uniform

atrial depolarization wave occurs

The ECG baseline usually shows irregular undulations

known as fibrillation (f) waves
 ATRIAL FIBRILLATION

•Associated with •Atrial and ventricular Causes :

severe underlying rates are rapid and totally
heart disease irregular Marked atrial enlrgement,
chronic AV valvular
•Paroxysmal •Ventricular rhythm insufficiency, DCM, PDA,
appears less irregular MI, TD, PS, VSD
•Loss of atrial kick,
rapid heart rate, •F waves of varying
reduce CO and amplitude replace normal
cause CHF. P waves

•QRS normal
ORIGIN OF SUPRAVENTRICULAR AND
VENTRICULAR ECTOPIC COMPLEXES
Ventricular Premature Complexes
An abnormal beat originating in the ventricles and occurring earlier than
expected in relation to the existing rhythm. A compensatory pause often
follows a VPC

Electrocardiographic features:
• As the site of depolarization is ventricular,there is no AV association
• P waves are not associated with the QRS complexes of the VPCs
• QRS complexes wide and bizarre, consistent with ventricular origin
• T wave polarity often reversed
Ventricular premature complexes
Ventricular premature complexes (VPCs, or PVCs)
originating below the AV node have a different and
usually wider QRS configuration compared with the
patient’s sinus complexes
Ventricular premature complexes
Ventricular premature complexes
Ventricular premature complexes
Causes are numerous and include structural heart disease,
familial in young German Shepherds, arrhythmogenic right
ventricular cardiomyopathy (boxer cardiomyopathy),
hypoxia, myocarditis, and drug induced (digoxin,
anesthesia).
Ventricular Tachycardia:

Three or more sequential VPCs, generally at a rate

>100/minute, constitutes ventricular tachycardia

Although some variation can occur, ventricular

tachycardia usually has regular QRS intervals
 Ventricular Tachycardia:
Runs of VPCs occurring in succession at a rate of usually
greater than 100 bpm. The inherent discharge rate of the
ventricle is approximately 40 to 50 bpm (seen with complete
heart block)

Electrocardiographic features:
• P waves not associated with QRS complexes
• QRS complexes wide and bizarre, consistent with ventricular origin
• Regular rhythm, as contrasted with atrial fibrillation and RBBB
 Ventricular tachycardia

Causes are the same as for VPCs:

• Ventricular tachycardia indicates significant heart
disease or systemic disease

• Cardiac output may be significantly impaired, and the

arrhythmia predisposes to ventricular fibrillation
Ventricular fibrillation
This lethal rhythm is characterized by multiple
reentrant circuits causing chaotic electrical activity in
the ventricles
Ventricular Fibrillation:
Completely irregular, chaotic variable fibrillation potentials, indicating lack of
organized ventricular depolarization and impending death

Electrocardiographic features:
• There is no evidence of organized cardiac depolarization
(absence of P- QRS-T waves)
• Wavy, undulating baseline
• Coarse ventricular fibrillation is characterized by large
wavelets
• Fine ventricular fibrillation is characterized by small wavelets
 Atrioventricular Junctional Tachycardia

Paroxysmal or sustained rhythm originating from AV nodal tissue

Electrocardiographic features:
• Rate is greater than 60 bpm (inherent rate of AV nodal tissue is approximately 40
bpm to 60 bpm)

• A regular rhythm

• Abnormal appearing P wave (often inverted in lead II), which may precede QRS,
be superimposed on QRS, or follow QRS complexes

• QRS complexes may be normal or may be widened secondary to aberrant

conduction.

Causes include digoxin toxicity and

structural heart disease
First-Degree Atrioventricular Block:

• Conduction through the AV node is delayed.

• Produces prolongation of the PR interval (more than 0.13 second for the dog, more
than 0.09 second for the cat)

• Causes include fibrosis of the AV node, vagal stimulation, and drug-induced

(digoxin) and electrolyte imbalance.

Isolated first degree AV block is not clinically significant but may be an

early indicator of progressive AV nodal dysfunction.
Second-Degree Atrioventricular Block
• There is intermittent blockage of conduction through the AV node.
• Following discharge of the SA node and atrial depolarization, there is no associated
ventricular depolarization

Electrocardiographic features :
• Absence of QRS-T complexes following P wave

• In Mobitz type I (Wenckebach) block, there is progressive prolongation of the PR

interval, followed by occurrence of second degree AV block

• In Mobitz type II block, there is second degree AV block without preceding

prolongation of the PR interval
Third-Degree Atrioventricular Block
(Complete Heart Block)
• All conduction through the AV node is blocked
• Atrial and ventricular depolarizations are no longer
coordinated and occur independently of one
another
•Ventricular depolarization is initiated by discharge
of a ventricular escape focus.

Electrocardiographic features
• There is no association between P waves and QRS-T complexes.
• P waves are of normal morphology and usually occur at a normal rate
• QRS complexes are of ventricular origin morphology
• Ventricular rate is typically 30 to 50 bpm
• Causes include fibrosis of the AV node, drug-induced (digoxin),
infiltrative disease, Rickettsial myocarditis, hyperkalemia

• Usually associated with clinical signs of weakness or collapse

•Complete AV block warrants implantation of a permanent pacemaker

in most cases
Low voltage QRS complex ST coving

Tall R waves

P Pulmonale
Atrial fibrillation
 Second-degree (Mobitz type II) AV block (4:1 to 7:1)

Before Atropine

After Atropine

Sinus Arrest
THANK YOU